<rss version='2.0'>

                    <channel>

                    <title><![CDATA[Cardiomyopathies]]></title>

                    <link>https://www.benthamscience.com</link>

                    <description>

                    RSS Feed for Disease Wise Article | BenthamScience

                    </description>

                    <generator>EurekaSelect (+http://eurekaselect.com)</generator>

                    <pubDate>Tue, 21 Jul 2026 19:46:34 +0000</pubDate>

                    <image>

                    <title><![CDATA[Cardiomyopathies]]></title>

                    <url>https://www.benthamscience.com</url>

                    <link>https://www.benthamscience.com</link>

                    </image><item><title><![CDATA[Pinworm (<i>Enterobius Vermicularis</i>) Infestation: An Updated Review]]></title><link>https://www.benthamscience.comarticle/138052</link><description><![CDATA[<p>Background: Pinworm infestation is an important public health problem worldwide, especially among children 5 to 10 years of age in developing countries with temperate climates. The problem is often overlooked because of its mild or asymptomatic clinical manifestations. </p> <p> Objectives: The purpose of this article was to familiarize pediatricians with the diagnosis and management of pinworm infestation. </p> <p> Methods: A search was conducted in August 2023 in PubMed Clinical Queries using the key terms “Enterobius vermicularis,” OR “enterobiasis,” OR “pinworm.” The search strategy included all clinical trials, observational studies, and reviews published within the past 10 years. Only papers published in the English literature were included in this review. The information retrieved from the above search was used in the compilation of the present article. </p> <p> Results: Enterobiasis is a cosmopolitan parasitosis caused by Enterobius vermicularis. It affects approximately 30% of children worldwide and up to 60% of children in some developing countries. Predisposing factors include poor socioeconomic conditions, inadequate sanitation, poor personal hygiene, and overcrowding. Children aged 5 to 14 years have shown the highest prevalence of enterobiasis.. Egg transmission is mainly by the fecal-oral route. Approximately 30 to 40% of infested patients do not show any clinical symptoms of the disease. For symptomatic patients, the most common presenting symptom is nocturnal pruritus ani. The diagnosis of E. vermicularis infection is best established by the cellophane tape test. The sensitivity of one single test is around 50%; however, the sensitivity increases to approximately 90% with tests performed on three different mornings. If a worm is visualized in the perianal area or the stool, a pathological examination of the worm will yield a definitive diagnosis. As pinworms and eggs are not usually passed in the stool, examination of the stool is not recommended. The drugs of choice for the treatment of pinworm infestation are mebendazole (100 mg), pyrantel pamoate (11 mg/kg, maximum 1 g), and albendazole (400 mg), all of the above-mentioned drugs are given in a single dose and repeated in two weeks. Mebendazole and albendazole are both adulticidal and ovicidal, whereas pyrantel pamoate is only adulticidal. Given their safety and effectiveness, mebendazole and albendazole are currently the best available drugs for the treatment of pinworm infestation. For pregnant women, pyrantel is preferred to mebendazole and albendazole. Treatment of all household members should be considered, especially if there are multiple or repeated symptomatic infections because reinfection is common even when effective medication is given. </p> <p> Conclusion: In spite of effective treatment of pinworm infestation, recurrences are common. Recurrences are likely due to repeated cycles of reinfection (particularly, autoinfection) because of the short life span of adult pinworms. Good personal hygiene, such as frequent handwashing, especially after bowel movements and before meals, clipping of fingernails, avoidance of finger-sucking, nail-biting, and scratching in the anogenital area, are important preventive measures. Treatment of all household members should be considered, especially if there are multiple or repeated symptomatic infections.</p>]]></description> </item><item><title><![CDATA[Electrocardiographic Patterns and Ejection Fraction in Patients with
Nonischemic Dilated Cardiomyopathy: A Cross-sectional Retrospective Study]]></title><link>https://www.benthamscience.comarticle/139404</link><description><![CDATA[<P>Background: The relationship between ECG changes in dilated nonischemic cardiomyopathy and ejection fraction (EF) is complex and poorly understood. Thus, this study aimed to identify the most common patterns of ECG associated with dilated nonischemic cardiomyopathy and their relationship to EF. <P> Methods: A retrospective cross-sectional study was conducted between 2019 and 2022, including 100 consecutive patients with nonischemic dilated cardiomyopathy. ECG data were rate, axis, left (LBBB) and right bundle branch block (RBBB), first-degree heart block, premature ventricular contractions, depth of S wave in leads V1 and V2, length of R wave in leads V2 and V6, the ratio of R/S in the lead V4, left ventricular hypertrophy (LVH), maximum R wave length in leads I, II, and III, poor R wave progression, ST-segment elevation, and T wave inversion. <P> Results: The most common ECG pattern associated with cardiomyopathy was T-wave inversion (47%). The EF was 23.9± 8.87% in patients with LBBB and 25.5± 8.07% in patients without LBBB (P= 0.361). In patients with T-wave inversion, the EF was 23.4± 8.21%, and it was 26.28± 8.35% in patients without T-wave inversion (P= 0.086). In patients with LVH, the EF was 23.89± 7.84%, and it was 25.5± 8.66% in patients without LVH (P= 0.354). A negative nonsignificant correlation existed between SV1, SV2, RV2, RV6, R/S V4, and maximum R in I, II, III, and EF. <P> Conclusions: The study showed that T-wave inversion was the most common pattern associated with dilated nonischemic cardiomyopathy. The study provided insight into the negative correlation between EF and SV1, SV2, RV2, RV6, R/S V4, and maximum R in I, II, and III, although it did not reach a significant level.</P>]]></description> </item><item><title><![CDATA[Congenital Abdominal Aortic Aneurysm: Presentation, Etiology, Diagnosis and
Management]]></title><link>https://www.benthamscience.comarticle/139402</link><description><![CDATA[Aortic aneurysms are common in adults due to atherosclerosis but are rare in children and young adults, often overlooked due to infrequent reporting. Acquired aneurysms are usually linked to factors like umbilical artery ligation, connective tissue diseases, or vasculitides. In contrast, the causes of congenital abdominal aortic aneurysms (AAA) remain unknown due to their extreme rarity. Only a few cases have been reported. Prompt diagnosis is essential when symptoms such as abdominal distention, vomiting, or abdominal pulsatility occur. Diagnosis is typically confirmed through ultrasonography and multi-slice spiral computed tomography angiographies (MCSTA). After detection, a comprehensive investigation is necessary to rule out acquired AAA causes. Managing congenital AAA requires a highly personalized approach, with early surgical repair using grafts as a recommended option. After an extensive analysis of numerous academic sources, we have comprehensively understood the epidemiology, clinical features, and diagnostic and treatment techniques for congenital abdominal aortic aneurysms.]]></description> </item><item><title><![CDATA[Artificial Intelligence and Cardiovascular Diseases]]></title><link>https://www.benthamscience.comarticle/138785</link><description><![CDATA[<p>Artificial intelligence (AI) has reshaped significant aspects of our lives, including its role in healthcare. <p> AI is a machine-based system that can make predictions, recommendations, and decisions influencing real or virtual environments of a given set of human-defined objectives. It is designed to operate with varying levels of autonomy. <p> Since cardiovascular medicine is rapidly progressing and new technologies are introduced to cardiovascular tools, AI has become valuable in cardiovascular medicine. This narrative review will discuss the general concept of AI and its role in diagnosing cardiovascular diseases, including ECG, echocardiography, cardiac CT, nuclear cardiology, cardiac MRI, cardiac catheterization, electrophysiology, heart failure, clinical decision support system, and face recognition.</p>]]></description> </item><item><title><![CDATA[A Review of Stem Cell Therapy in Ischemic Heart Disease, Where are We Now?]]></title><link>https://www.benthamscience.comarticle/133928</link><description><![CDATA[<P>Background: Regenerative therapies to rejuvenate the heart have a significant appeal for researchers. Preliminary findings from pre-clinical studies suggest that bone marrow cells may have reparative and regenerative effects on heart muscles, creating a ripe area for research. Many generations of stem cells used in pre-clinical and early clinical studies have shown promising but variable results. <P> Objective: The current review article discusses the dilemmas in applying stem cell therapy to cardiovascular diseases and possible strategies to make it feasible. <P> Methods: The field of regenerative therapies continued to progress with second-generation cells, third-generation cells, combination cell therapy, and the use of cell products alone. Research showed promising positive results in multiple randomized phases 1, 2, and 3 clinical trials in addition to numerous meta-analyses. The gaps in knowledge included stem-cell sources, their delivery routes, dosing, types of cells, and the indicated cardiac conditions. <P> Results: The results from the latest randomized clinical trials, namely the Dream-HF, showed improved left ventricle function, symptoms, and overall survival. Studied patient populations include post-myocardial infarction (MI), ischemic/non-ischemic cardiomyopathy, intractable/microvascular angina, and cardiac surgery for congenital and valvular heart disease. The phase 3 DREAM-HF trial did not meet the primary heart failure endpoint of reducing hospital admission. Still, it showed a clinically significant reduction in major adverse cardiovascular events (MACE), including recurrent MI and stroke, by 60%. A 60% reduction in cardiovascular mortality and a 79% reduction in cardiovascular mortality in patients with evidence of inflammation (high CRP). The latter finding suggests a more anti-inflammatory effect. This effect was much higher than that observed in the PARADIGM-HF trial, which showed a 20% relative risk reduction in cardiovascular mortality. By combining the results of the DREAM-HF trial with MSC-HF, ixCELL-DCM, CONCERT-HF, and REGENERATE-DCM, the potential for clinical applications of cell therapy is promising. <P> Conclusion: There is a promising role for cell therapy in the management of cardiovascular diseases. Results of trials in the setting of heart failure are more encouraging in both ischemic and non-ischemic cardiomyopathy. This is in contrast with acute myocardial infarction, where the results have been variable. Amongst all the various cell types tested MSCs show the most significant promise for treating HF.</P>]]></description> </item><item><title><![CDATA[Tertiary Hyperparathyroidism and Extra Skeletal Calcification in End Stage
Kidney Disease Patients: Case-series and Literature Review]]></title><link>https://www.benthamscience.comarticle/135967</link><description><![CDATA[<p>Background: Tertiary hyperparathyroidism (THPT) is a well-known complication of end-stage kidney disease (ESKD), resulting from a loss of functional renal tissue with subsequent alterations in calcium and phosphate metabolism. Tertiary hyperparathyroidism reflects severe parathyroid hyperplasia with autonomous excessive secretion of parathyroid hormone (PTH) that is no longer responsive to the concentration of plasma calcium and leads to abnormal bone remodelling, soft tissue calcifications, vasculopathy, and other systemic complications. <p> Case Presentation: The authors, hereby, highlight varied presentations of tertiary hyperparathyroidism (THPT) by presenting 3 interesting cases, describing their clinical course and outcomes. Through sharing these experiences and insights, we hope to contribute to a better understanding of THPT and its optimal management in patients with ESKD. <p> Conclusion: THPT can have a significant impact on patient health and quality of life. Despite the widespread use of interventions, such as vitamin D analogues, calcimimetics and parathyroidectomy, THPT remains a significant clinical challenge for patients with ESKD.</p>]]></description> </item><item><title><![CDATA[RBM3 Accelerates Wound Healing of Skin in Diabetes through ERK1/2
Signaling]]></title><link>https://www.benthamscience.comarticle/135223</link><description><![CDATA[<p>Background: With the increasing risk of infections and other serious complications, the underlying molecular mechanism of wound healing impairment in diabetes deserves attention. Cold shock proteins (CSPs), including CIRP and RBM3 are highly expressed in the skin; however, it is unknown whether CSPs are involved in the wound-healing impairment of diabetic skin. <p> Objectives: The objective of this study is to investigate the effects of RBM3 on skin wound healing in diabetes. <p> Methods: In vitro experiments, western blot assay was used to test the levels of proteins in HaCaT cells treated with different concentrations of glucose. RBM3 was over-expressed in HaCaT cells using lentivirus particles. Cell viability was analyzed by Cell-Counting Kit-8 assay and colony formation assay. The migration of HaCaT cells at different concentrations of glucose was evaluated by wound healing assay. In vivo experiments, the mouse model of diabetes was established by intraperitoneal injection of streptozotocin. Four weeks later, the mice were anesthetized by intraperitoneal injection of pentobarbital sodium for skin tissue collection or wound healing experiments. RBM3 knockout mice were established by removing exons 2–6 using the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 technique and then used in skin wound healing experiments with or without diabetic stress. <p> Results: In this study, the expression of RBM3, rather than CIRP, was altered in the skin of diabetic specimens, and the RBM3’s overexpression accelerated the cell viability and proliferation of HaCaT cells under high glucose conditions. RBM3 deficiency caused delayed wound healing in RBM3 knockout in diabetic conditions. Moreover. RBM3 enhanced the ERK1/2 signaling pathway, and its inhibitor FR180204 blocked the beneficial effect of RBM3 overexpression on skin wound healing in diabetes. <p> Conclusion: RBM3 activated the ERK1/2 signal to facilitate skin wound healing in diabetes, offering a novel therapeutic target for its treatment.</p>]]></description> </item><item><title><![CDATA[A Comprehensive Review of Essential Aspects of Molecular Pathophysiological
Mechanisms with Emerging Interventions for Sarcopenia in Older People]]></title><link>https://www.benthamscience.comarticle/130060</link><description><![CDATA[<P>Background: As people age, physical impairments may have a deleterious role on skeletal muscles. Sarcopenia Clinical Practice Guidelines 2017 and the European Working Group on Sarcopenia in older people are two organizations that have published essential guidelines on the definition of “Sarcopenia”. Sarcopenia is a geriatric syndrome, characterized by skeletal muscle mass degeneration brought on by ageing, which lowers muscular function and quality. Moreover, Sarcopenia can be classified as primary or age-associated Sarcopenia and secondary Sarcopenia. Also, secondary Sarcopenia occurs when other diseases such as diabetes, obesity, cancer, cirrhosis, myocardial failure, chronic obstructive pulmonary disease, and inflammatory bowel disease also contribute to muscle loss. Furthermore, Sarcopenia is linked with a high risk of negative outcomes, considering a gradual reduction in physical mobility, poor balance, and increased fracture risks which ultimately leads to poor quality of life. <P> Objective: In this comprehensive review, we have elaborated on the pathophysiology, and various signaling pathways linked with Sarcopenia. Also, discussed the preclinical models and current interventional therapeutics to treat muscle wasting in older patients. <P> Conclusion: In a nutshell, a comprehensive description of the pathophysiology, mechanisms, animal models, and interventions of Sarcopenia. We also shed light on pharmacotherapeutics present in clinical trials which are being developed as potential therapeutic options for wasting diseases. Thus, this review could fill in the knowledge gaps regarding Sarcopenia-related muscle loss and muscle quality for both researchers and clinicians.</P>]]></description> </item><item><title><![CDATA[A Review of the Dual Role of MicroRNA-21 in Cardiovascular Diseases: Risk
Factor or a Potential Therapeutic Target]]></title><link>https://www.benthamscience.comarticle/138046</link><description><![CDATA[Cardiovascular diseases (CVD) are the number one reason for morbidity and mortality in the modern world, and their incidence is increasing at an incredible pace. Increasing evidence has shown the significant functions of microRNAs in the cardiovascular system and has highlighted their potential application as a new era of diagnostic and therapeutic targets for CVD that can improve the prognosis and life expectancy of patients. Among more than 2,000 microRNAs, microRNA-21 (miR-21) is highly expressed in human hearts and has earned the interest of researchers as a potential biomarker in a wide range of common heart conditions. Here, we summarized recent research progress regarding the significant role of miR-21 in CVD, focusing on cardiotoxicity, heart arrhythmias, cardiomyopathies, and hypertension. Several signaling pathways (TGF-&#946;1/Smad2 signaling, FGFR1/FGF21/PPAR&#947;, NF-&#954;B/miR-21/SMAD7, miR-21/SPRY1/ERK/mTOR …) and molecular targets (BTG2, PDCD4, PTEN, STAT3…) were reported to be controlled, at least partially, by miR-21 and are linked to CVD pathogenesis. Most investigations highlighted miR-21 cardioprotective functions in heart injury, while some other studies showed that this miR is elevated in the serum/tissue of patients, promoting fibrosis and cardiac dysfunction. This dual role can be explained by the fact that miR-21 has multiple regulatory functions depending on the microenvironment, downstream signaling, and target genes, which indicates that cell-type-specific investigations should receive more attention. With further investigations, miR-21 can be considered a novel tailored therapy with favorable outcomes.]]></description> </item><item><title><![CDATA[Nrf2 Mediates Effect of Resveratrol in Ischemia-reperfusion Injury]]></title><link>https://www.benthamscience.comarticle/138158</link><description><![CDATA[Ischemia-Reperfusion Injury (IRI) is a paradoxical phenomenon where removing the source of injury can cause additional damage. Ischemia reduces ATP production and intracellular pH, reducing oxidative reactions, increasing lactic acid release, and activating anaerobic metabolism. Reperfusion restores aerobic respiration and increases ROS production, leading to malfunction of transmembrane transport, activation of proteases, DNA dissolution, and protein denaturation, leading to apoptotic cell death. Nrf2 is a transcription factor that regulates cellular inflammation and oxidative responses. It is activated by oxidants and electrophiles and enhances detoxifying enzyme expression, maintaining redox homeostasis. It also activates ARE, which activates several ARE-regulated genes that favor cell survival by exhibiting resistance to oxidants and electrophiles. Nrf2 regulates the antioxidant defense system by producing phase II and antioxidant defense enzymes, including HO-1, NQO-1, gglutamylcysteine synthetase, and rate-limiting enzymes for glutathione synthesis. Nrf2 protects mitochondria from damage and supports mitochondrial function in stress conditions. Resveratrol is a stilbene-based compound with a wide variety of health benefits for humans, including antioxidant, anticarcinogenic, antitumor, and estrogenic/antiestrogenic. Resveratrol protects against IRI through several signaling pathways, including the Nrf2/ARE pathway. Here, we review the studies that investigated the mechanisms of resveratrol protection against IRI through modulation of the Nrf2 signaling pathway.]]></description> </item><item><title><![CDATA[An Enzyme-responsive Porphyrin Metal-organic Framework Nanosystem for Targeted and Enhanced Synergistic Cancer Photo-chemo Therapy]]></title><link>https://www.benthamscience.comarticle/138826</link><description><![CDATA[<p>Background: The clinical efficiency of photodynamic therapy (PDT) in combination with chemotherapy has proven to be a promising strategy for tumor treatment, yet is restricted by the high glutathione (GSH) concentration at the tumor site and nonspecific drug targeting. </p> <p> Objective: The goal of the current research was to create a biocompatible GSH-depleting and tumor- targeting nanoparticle (denoted as DOX/CA@PCN-224@HA) for the combined photodynamic and chemo photo-chemo) therapy. </p> <p> Methods: The nanoparticles were characterized by transmission electron microscopy (TEM). A UV-vis spectrophotometer was used to measure the drug loading efficiency (DE) and encapsulation efficiency (EE). The GSH-depleting ability was measured using Ellman's test. Confocal laser scan microscopy (CLSM) was used to assess the cellular uptake. MTT was adopted to evaluate the cytotoxicity of DOX/CA@PCN-224@HA against 4T1 cells. </p> <p> Results: The altered PCN-224 showed excellent monodispersing with a dimension of approximately 193 nm ± 2 nm in length and 79 nm ± 3 nm in width. The larger and spindle grid-like structure of PCN-224 obtains better dual-drug loading ability (DOX: 20.58% ± 2.60%, CA: 21.81% ± 1.98%) compared with other spherical PCN-224 nanoparticles. The ultimate cumulative drug release rates with hyaluronidase (HAase) were 74% ± 1% (DOX) and 45% ± 2% (CA) after 72 h. DOX/CA@PCN-224@HA showed GSH-consuming capability, which could improve the PDT effect. The drug-loaded nanoparticles could accurately target 4T1 cells through biological evaluations. Moreover, the released DOX and CA display cooperative effects on 4T1 cells <i>in vitro</i>. DOX/CA@PCN-224@HA nanoparticles showed inhibition against 4T1 cells with an IC<sub>50</sub> value of 2.71 μg mL<sup>-1</sup>. </p> <p> Conclusion: This nanosystem displays great potential for tumor-targeted enhanced (photo-chemo) therapy.</p>]]></description> </item><item><title><![CDATA[DHA and EPA in Sickle Cell Disease Favor Clinical Improvement and Contribute to Better Quality of Life: A Qualitative Systematic Review]]></title><link>https://www.benthamscience.comarticle/138533</link><description><![CDATA[<p>Background: Sickle cell disease is a severe genetic disorder, and searching for therapeutic strategies is indispensable for prolonged and improved life for people affected by this condition. </p> <p> Objectives: This qualitative systematic review aimed to highlight the therapeutic potential of omega- 3 (n-3) in people with sickle cell disease. </p> <p> Methods: The search was performed by combining sickle cell disease and n-3 descriptors in DeCS/ MeSH databases, including Scopus, PubMed, ScienceDirect, Web of Science, and Virtual Health Library. The risk of bias assessment in the primary studies was performed using the Cochrane risk of bias tool for randomized controlled trials. The evidence quality was evaluated using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) tool. </p> <p> Results: From the 187 records identified, seven were selected for data collection. Based on the evidence, n-3 supplementation contributes to lower activation of pro-inflammatory biomarkers, improves the concentration of docosahexaenoic and eicosapentaenoic acids in the erythrocyte membrane, provides better hemostatic response, and helps in vaso-occlusive crisis, pain episodes, and hospitalization reduction. </p> <p> Conclusion: The findings suggest that n-3 adjuvant therapy favors the clinical and general aspects of people with sickle cell disease.</p>]]></description> </item><item><title><![CDATA[Misery of Long Haulers of COVID-19 - A Review]]></title><link>https://www.benthamscience.comarticle/129941</link><description><![CDATA[<p>Background: Early in December 2019, Wuhan City, Hubei Province, China, had an epidemic of the Coronavirus illness 2019 (COVID-19), which was brought on by a brand-new severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2). The epidemic was deemed a Public Health Emergency of International Concern by the World Health Organization on January 30, 2020. Many governments have implemented a range of control measures as a result of perceived illness risk. <p> Objectives: The pandemic revealed that COVID-19 affects a variety of organs in addition to the lungs, including the heart and brain, raising the risk of long-term health consequences. The illness can affect someone's health even after recovery in a variety of ways. The long-term effects of COVID-19 on locals are still being researched. The objective is to compile knowledge regarding the virus and the present Post pandemic complications in Long Haulers. <p> Methods: We reviewed the body of publicly available literature. To discover publications published between December 2019 and October 2020, we conducted a systematic search utilizing the keywords in online databases such as Pub Med, Scopus, Science Direct, Up to Date, and Web of Science. The review includes peer-reviewed original publications published that matched the qualifying requirements. <p> Results: Although the majority of patients recovered quickly after receiving COVID-19, the possibility of long-term issues induced by COVID-19 necessitates the search for and research of its late consequences. This article aims to provide a comprehensive assessment of COVID-19 late complications in order to determine how prevalent these symptoms are and who is most likely to be impacted. <p> Conclusion: There are a number of difficulties with the COVID-19 pandemic that has yet to be resolved. Review of the literature reported several long-lasting clinical problems that affect different phases of health, including chronic fatigue, reduced physical capacity, muscle weakness, increased depression, anxiety, post-traumatic stress disorder and sleep problems. A complete turndown in quality of life has been observed even one year after major Coronavirus outbreaks. <p> The pandemic revealed that COVID-19 affects a variety of organs in addition to the lungs, including the heart and brain, raising the risk of long-term health consequences even after years making them to be “Long Haulers”. <p> The causal agent, pathogenesis, immunological responses, epidemiology, diagnosis, therapy, and management of the disease, as well as control and preventive efforts, are all included in this review of the literature.</p>]]></description> </item><item><title><![CDATA[Role of Multi-parameter-based Cardiac Magnetic Resonance in the Evaluation
of Patients with Coronary Heart Disease Combined with Heart Failure]]></title><link>https://www.benthamscience.comarticle/139200</link><description><![CDATA[<P>Background: Coronary Heart Disease (CHD) is one of the most common types of cardiovascular disease, and Heart Failure (HF) is an important factor in its progression. We aimed to evaluate the diagnostic value and predictors of multiparametric Cardiac Magnetic Resonance (CMR) in CHD patients with HF. <P> Methods: The study retrospectively included 145 CHD patients who were classified into CHD (HF+) (n = 91) and CHD (HF–) (n = 54) groups according to whether HF occurred. CMR assessed LV function, myocardial strain and T1 mapping. Multivariate linear regression analyses were performed to identify predictors of LV dysfunction, myocardial fibrosis, and LV remodeling. <P> Results: CHD (HF+) group had impaired strain, with increased native T1, ECV, and LVM index. The impaired strain was associated with LVM index (p < 0.05), where native T1 and ECV were affected by log-transformed amino-terminal pro-B-type natriuretic peptide (NT-proBNP) levels. ROC analysis showed the combination of global circumferential strain (GCS), native T1, and LVM had a higher diagnostic value for the occurrence of HF in CHD patients. Meanwhile, log-transformed NT-proBNP was an independent determinant of impaired strain, increased LVM index, native T1 and ECV. <P> Conclusion: HF has harmful effects on LV systolic function in patients with CHD. In CHD (HF+) group, LV dysfunction is strongly correlated with the degree of LV remodeling and myocardial fibrosis. The combination of the three is more valuable in diagnosing HF than conventional indicators.</P>]]></description> </item><item><title><![CDATA[Differences in the Fat Attenuation Index Ratio of Pericoronary Adipose Tissue
And Aortic Root Epicardial Adipose Tissue in Various Plaques]]></title><link>https://www.benthamscience.comarticle/135754</link><description><![CDATA[<p>Background: The fat attenuation index (FAI) of pericoronary adipose tissue is associated with coronary inflammatory reactions. <p> Objective: This study aimed to analyze the difference in the FAI ratio between pericoronary adipose tissue volume and aortic root epicardial adipose tissue volume (AO-EATV) using computed tomography (CT) in various plaques. <p> Methods: In total, 645 coronary artery CT angiogram images from 215 patients were collected. The types and number of coronary plaques were recorded, and the plaque volume and pericoronary FAI of each branch were compared between the groups. The ratio of the FAI in branches with or without plaques to the AO-EATV was determined and statistically analyzed between the groups. <p> Results: No significant difference in the plaque volume among the left anterior descending (LAD), left circumflex (LCX), and right coronary artery (RCA) (P > 0.05) as well as in the FAI was observed among various plaque groups (P > 0.05). FAI[LAD]/AO-EATV was in the following order: noncalcified plaques (0.70 ± 0.06) &#60; mixed plaques (0.72 ± 0.06) &#60; calcified plaques (0.73 ± 0.08) &#60; no plaques (0.74 ± 0.07); FAI[LCX]/AOEATV was in the following order: noncalcified plaques (0.71 ± 0.06) &#60; mixed plaques (0.72 ± 0.08) &#60; calcified plaques (0.73 ± 0.09) &#60; no plaques (0.74 ± 0.06); and FAI[RCA]/AO-EATV was in the following order: noncalcified plaques (0.71 ± 0.06) &#60; mixed plaques (0.73 ± 0.07) &#60; calcified plaques (0.74 ± 0.07) &#60; no plaques (0.75 ± 0.09); the differences were statistically significant in each group (P = 0.041, 0.043, and 0.028, respectively). <p> Conclusion: Compared to simply comparing FAI, FAI/AO-EATV varied in the coronary arteries in various plaque groups. FAI/AO-EATV was lower in noncalcified or mixed plaques and was associated with coronary inflammatory reactions.]]></description> </item><item><title><![CDATA[A Comprehensive Review of <i>Abroma Augusta</i> (Devil's Cotton): Phytochemical
Constituents, Ethnomedicinal Applications, and Pharmacological Properties]]></title><link>https://www.benthamscience.comarticle/136596</link><description><![CDATA[The nutritional and therapeutic potential of medicinal plants is constantly being investigated. This is especially relevant in today's world, where an increasing number of people are turning to complementary and alternative therapies to address their health-related concerns. Traditional knowledge, as a valuable resource, plays a crucial role in the development of new herbal medicines. <i>Abroma augusta</i> stands out as one such medicinal plant that has a rich history of use in traditional medicine. It has been employed to address a wide spectrum of health issues, including diabetes, menstrual irregularities, respiratory problems, musculoskeletal disorders, urinary ailments, and sexual dysfunctions, among others. While various parts of this plant species are believed to possess pharmacological properties, the active compounds and underlying mechanisms remain largely unexplored. To facilitate the development of innovative drugs for the benefit of individuals, this study places significant emphasis on delving into the phytochemical and ethnomedicinal attributes of <i>A. augusta</i>. Moreover, it seeks to bolster its findings with scientifically validated pharmacological investigations conducted through both <i>in vivo</i> and <i>in vitro</i> methodologies.]]></description> </item><item><title><![CDATA[Current Trends in Feature Extraction and Classification Methodologies of
Biomedical Signals]]></title><link>https://www.benthamscience.comarticle/130073</link><description><![CDATA[Biomedical signal and image processing is the study of the dynamic behavior of various bio-signals, which benefits academics and research. Signal processing is used to assess the behavior of analogue and digital signals for the assessment, reconfiguration, improved efficiency, extraction of features, and reorganization of patterns. This paper unveils hidden characteristic information about input signals using feature extraction methods. The main feature extraction methods used in signal processing are based on studying time, frequency, and frequency domain. Feature exaction methods are used for data reduction, comparison, and reducing dimensions, producing the original signal with sufficient accuracy with a structure of an efficient and robust pattern for the classifier system. Therefore, an attempt has been made to study the various feature extraction methods, feature transformation methods, classifiers, and datasets for biomedical signals.]]></description> </item><item><title><![CDATA[T1 Mapping and Amide Proton Transfer Weighted Imaging for Predicting
Lymph Node Metastasis in Patients with Rectal Cancer]]></title><link>https://www.benthamscience.comarticle/138395</link><description><![CDATA[<p>Background: Accurate preoperative judgment of lymph node (LN) metastasis is a critical step in creating a treatment strategy and evaluating prognosis in rectal cancer (RC) patients. <p> Objective: This study aimed to explore the value of T1 mapping and amide proton transfer weighted (APTw) imaging in predicting LN metastasis in patients with rectal cancer. <p> Methods: In a retrospective study, twenty-three patients with pathologically confirmed rectal adenocarcinoma who underwent MRI and surgery from August 2019 to August 2021 were selected. Then, 3.0T/MR sequences included conventional sequences (T1WI, T2WI, and DWI), APTw imaging, and T1 mapping. Patients were divided into LN metastasis (group A) and non-LN metastasis groups (group B). The intra-group correlation coefficient (ICC) was used to test the inter-observer consistency. Mann-Whitney U test was used to compare the differences between the two groups. Spearman correlation analysis was performed to evaluate the correlation between T1 and APT values. Logistic regression and receiver operating characteristic (ROC) curve analyses were performed to assess the differential performance of each parameter and their combination. The difference between AUCs was compared using the DeLong test. <p> Results: The APT value in patients with LN metastasis was significantly higher than in those without LN metastasis group (P=0.020). Also, similar results were observed for the T1 values (P=0.001). The area under the ROC curve of the APT value in the prediction of LN metastasis was 0.794; when the cutoff value was 1.73%, the sensitivity and specificity were 71.4% and 88.9%, respectively. The area under the ROC curve of the T1 value was 0.913; when the cutoff value was 1367.36 ms, the sensitivity and specificity were 78.6% and 100.0%, respectively. The area under the ROC curve of T1+APT was 0.929, with a sensitivity of 78.6% and specificity of 100.0%. <p> Conclusion: APT and T1 values show great diagnostic efficiency in predicting LN metastasis in rectal cancer.</p>]]></description> </item><item><title><![CDATA[Feasibility of Weight-based Tube Voltage and Iodine Delivery Rate for
Coronary Artery CT Angiography]]></title><link>https://www.benthamscience.comarticle/139015</link><description><![CDATA[<p>Purpose: The objective of this study was to evaluate the feasibility of weight-based tube voltage and iodine delivery rate (IDR) for coronary artery CT angiography (CCTA). <p> Methods: A total of 193 patients (mean age: 58 ± 12 years) with suspected coronary heart disease indicated for CCTA between May and October 2022 were prospectively enrolled. The subjects were divided into five groups according to body weight: < 60 kg, 60 – 69 kg, 70 – 79 kg, 80 – 89 kg, and ≥ 90 kg. The tube voltage and IDR settings of each group were as follows: 70 kVp/0.8 gI/s, 80 kVp/1.0 gI/s, 80 kVp/1.1 gI/s, 100 kVp/1.5 gI/s, and 100 kVp/1.5 gI/s, respectively. Objective image quality data included the CT value and standard deviation (noise) of the aortic root (AR), the proximal left anterior descending branch (LAD), and the distal right coronary artery (RCA), as well as the signal-to-noise ratio and contrast-to-noise ratio of the LAD and RCA. Subjective image quality assessment was performed based on the 18-segment model. Contrast and radiation doses, as well as effective dose (ED), were recorded. All continuous variables were compared using either the one-way ANOVA or the Kruskal-Wallis rank sum test. <p> Results: No significant differences were observed in all objective and subjective parameters of image quality between the groups (P > 0.05). However, significant differences in contrast and radiation doses were observed (P < 0.05). The contrast doses across the weight groups were 27 mL, 35 mL, 38 mL, 53 mL, and 53 mL, respectively, while the ED were 1.567 (1.30, 2.197) mSv, 1.53 (1.373, 1.78) mSv, 2.113 (1.963, 2.256) mSv, 4.22 (3.771, 4.483) mSv, and 4.786 (4.339, 5.536) mSv, respectively. <p> Conclusion: Weight-based tube voltage and IDR yielded consistently high image quality, and allowed for further reduction in contrast and radiation exposure during CCTA for coronary artery diseases.</p>]]></description> </item><item><title><![CDATA[Choosing the Adaptive Cardiac Phase for Assessing Cardiac Dimensions Using
Cardiac Computed Tomography for Heart Disease]]></title><link>https://www.benthamscience.comarticle/139956</link><description><![CDATA[<P>Background: Cardiac chamber dimensions and left ventricle (LV) wall thickness change with the cardiac cycle, in which researchers have set different time points for systole and diastole. <P> Objective: This study aimed to provide characteristics of normal heart and choose the correct cardiac cycle to measure maximum cardiac parameters for cardiovascular disease. <P> Methods: The parameters of left atrium (LA), LV, right atrium (RA), and right ventricle (RV), as well as the wall thickness of LV, were measured in different cardiac phases using cardiac computed tomography (CT). Then, their differences in different phases and the correlation between these parameters and traditional risk factors were analyzed. In addition, receiver operator characteristic curve (ROC) analyses was performed to estimate LA enlargement. <P> Results: The dimensions of LA and RA as well as the wall thickness of LV reached the maximum at the phase of 35% – 45%, while the dimensions of LV and RV reached the maximum at 95% – 5%. However, the changes of LA-B (antero-posterior diameter), LV-D1 (basal dimension), RA-B (minor dimension), and RV-D2 (mid cavity dimension) were relatively more stable than other diameters during the cardiac cycle. The maximum LA-B diameter, LV-D1 diameter, RA-B diameter, and RV-D2 diameter as well as the maximum interventricular septum thickness were acquired. Heart rate (HR) and smoking were potential indicators of LV-D2 (mid cavity dimension), while HR and LV myocardial mass were potential indicators of LV-D3 (apical-basal dimension). In phase 45%, the cut-off value of LA-B was 37.12 mm, with high sensitivity for predicting LA enlargement. <P> Conclusion: Choosing the adaptive cardiac phase for evaluating cardiac chamber dimensions and wall thickness obtained by cardiac CT could provide a more accurate clinical measurement of the heart.</P>]]></description> </item><item><title><![CDATA[Coronary Cameral Fistula Disclosed by Echocardiography: A Case Report of
Typical Findings and Literature Review]]></title><link>https://www.benthamscience.comarticle/130157</link><description><![CDATA[<p>Background: Coronary cameral fistula is a rare cardiovascular anomaly, and usually needs advanced image modalities, such as computerized tomography and/or angiography, to confirm its existence. A few reports in the literature have addressed the role of medical ultrasound in the diagnosis of this disease, without a comprehensive summary of all the valuable echocardiographic features in its diagnosis. <p> Case Presentation: Hereby, we presented an 80-year-old lady with exertional dyspnea and angina. We diagnosed coronary cameral fistula from the left anterior descending artery into the left ventricle by echocardiography with “intramyocardial vascular channel and the diastolic flow”, and “multiple diastolic flow jets into heart chamber from heart wall”. We confirmed the diagnosis with coronary angiography later. In the discussion, we make a comprehensive summary to conclude all the echocardiographic findings of this disease into 3 categories. <p> Conclusion: We believe the identification of those findings will prompt the early diagnosis of this rare anomaly.</p>]]></description> </item><item><title><![CDATA[Acute Mesenteric Ischemia: The Diagnostic Value of QT Parameters and their
Relationship with CT Findings]]></title><link>https://www.benthamscience.comarticle/127251</link><description><![CDATA[<p>Background: One of the greatest challenges in the diagnosis of acute mesenteric ischemia (AMI) is the lack of specific laboratory tests that support multidetector computed tomography (CT). Our aim is to investigate the diagnostic value of electrocardiographic QT parameters in AMI and their relationship with CT findings. <p> Materials and Methods: Patients who were admitted to the emergency department with abdominal pain were recruited retrospectively from the hospital information system. Grouping was carried out on the basis of AMI (n=78) and non-AMI (n=78). In both groups, the corrected QT (QTc) and QT dispersion (QTD) were measured on electrocardiographs, and the qualitative and quantitative CT findings were evaluated on CT examinations. <p> Results: The QTc and QTD values were higher in the AMI group. The median QTc values were 456.16 (IQR: 422.88-483.16) for the AMI group and 388.83 (IQR: 359.74-415.83) for the control group (p&#60;0.001), and the median QTD values were 58 (IQR: 50.3-68.25) for the AMI group and 46 (IQR: 42-50) for the control group (p&#60;0.001). <p> In the CT analysis, the QTc values were significantly higher among AMI patients, with images of paper-thin bowel walls and the absence of bowel wall enhancement (p=0.042 and p=0.042, respectively). Meanwhile, the QTD values were significantly higher among patients with venous pneumatosis findings on CT (p=0.005). In the regression analysis, a significant relationship was found between the QT parameters and AMI (p&#60;0.001). For QTc, an AUC of 0.903 (95% CI: 0.857-0.950, p&#60;0.001), a sensitivity of 80.8%, and a specificity of 82.3% were found. For QTD, an AUC of 0.821 (95% CI: 0.753-0.889, p&#60;0.001), a sensitivity of 73.1%, and a specificity of 82.3% were found. <p> Conclusion: We found the QTc and QTD values to be significantly higher among AMI patients. Furthermore, we found a significant relationship between the CT findings and QTc and QTD and a significant relationship between survival and QTc in the AMI group.</p>]]></description> </item><item><title><![CDATA[The Effect of Contrast-enhanced Ultrasound <i>via</i> Vessels and Surgical Drains
Guidance Percutaneous Catheter Drainage in the Treatment of Pyogenic Liver
Abscess]]></title><link>https://www.benthamscience.comarticle/138998</link><description><![CDATA[<p>Background: Pyogenic liver abscess (PLA) is a purulent disease caused by microbial contamination of liver parenchyma and includes amoebic liver abscess, fungal liver abscess, and the most common bacterial liver abscess. <p> Objective: Explore the efficacy of contrast-enhanced ultrasound (CEUS) via vessels and surgical drain guidance percutaneous catheter drainage (PCD) in the treatment of pyogenic liver abscesses (PLA). <p> Materials and Methods: A total of 86 PLA patients who underwent PCD treatment in our hospital from May 2018 to February 2023 were retrospectively selected. Of them, 41 patients were treated under intravenous CEUS guidance (Control group), and 45 patients were treated under CEUS via vessels and surgical drain guidance (study group). Perioperative characteristics, treatment effectiveness, and incidence of complications were analyzed and compared between groups. <p> Results and Discussion: The duration of surgery, drainage, white blood cell recovery, body temperature recovery, and hospitalization in the study group were longer than those in the control group (P<0.05). The total effective rate of the study group (95.56%) was higher than that of the control group (80.49%) (P<0.05). The incidence of complications in the study group (4.44%) was lower than that in the control group (19.51%) (P<0.05). <p> Conclusion: Compared with intravenous CEUS alone, treatment under CEUS via vessels and surgical drains-guided PCD was associated with shorter surgical time, faster recovery, better treatment effect, lower risk of complications, and ensured treatment safety in PLA patients.</p>]]></description> </item><item><title><![CDATA[Early Markers of Sepsis Cardiomyopathy in Murine Models by
Echocardiography]]></title><link>https://www.benthamscience.comarticle/131329</link><description><![CDATA[<p>Background: Strain echocardiography (SE) is a procedure for analyzing myocardial dysfunction that is known to be less dependent on preload and afterload of heart function. Unlike dimension-based parameters, like ejection fraction (EF) and fractional shortening (FS), SE measures cardiac function by tracking cardiac tissue deformation and anomalies throughout the cardiac cycle. Although SE is proven to locate myocardial ailments in various heart diseases, few studies exist regarding using SE relevant to sepsis pathophysiology. <p> Objective: The study aimed to calculate the myocardial strain and strain rates, like longitudianl strain (LS), global radial strain (GRS), and global longitudinal strain (GLS), and to show these to be reduced earlier in cecal ligation and puncture (CLP) and lipopolysaccharide (LPS)-induced sepsis in coordination with an elevation of pro-inflammatory cytokines. <p> Methodology: Wild-type mice C57BL/6J (WT) were taken in this study and classified as CLP, LPS, and control groups. CLP surgery and LPS injection were given to induce sepsis. Endotoxemic septic shock was induced by intraperitoneal (IP) injection of LPS Escherichia coli. <p> Echocardiography short axis views (SAX), longitudinal strain (LS), global circumferential strain (GCS), and global radial strain (GRS) were measured from the anterior and posterior positions of the septal and lateral walls of the heart. Real-time polymerase chain reaction (RT-PCR) was performed to evaluate post-CLP and LPS to analyze cardiac pro-inflammatory cytokines expressions. Inter- and intra-observer variables were tested by Bland-Altman analyses (BA). All data analysis was performed by GraphPad Prism 6 software. p<0.05 was taken as statistically significant. <p> Results: After 48 hours following CLP and LPS-induced sepsis, a significant declination in both longitudinal strain and strain rate (LS and LSR) was identified in the CLP and LPS groups compared to the control group. Strain depression in sepsis was linked with the up-regulation of proinflammatory cytokines in RT-PCR analysis. <p> Conclusion: In the present study, we found myocardial strain and strain rate parameters, like LS, GRS, and GLS, to be reduced after CLP and LPS-induced sepsis in coordination with the elevation of pro-inflammatory cytokines.</p>]]></description> </item><item><title><![CDATA[Evaluation of the Atherogenic Effect of Covid-19 Pneumonia on Coronary and
Carotid Arteries in Patients who Recovered from the Disease]]></title><link>https://www.benthamscience.comarticle/139014</link><description><![CDATA[<P>Background: Acute inflammation induced by COVID-19 may lead to atherosclerotic plaque development or complicate existing plaque. In this study, we aimed to determine the atherogenic effect of COVID-19 pneumonia, confirmed by thoracic computed tomography, on coronary and carotid arteries in patients who recovered from the disease. <P> Methods: Our study included patients who were diagnosed with COVID-19 in our hospital at least 1 year ago, recovered, and then underwent coronary CT angiography with suspected coronary artery disease. The aim was to evaluate the burden of atherosclerotic plaque in the coronary arteries of these patients who underwent coronary CT angiography. <P> Results: Patients were assigned to 3 groups according to the results of the CT scan. Group 1 included patients in the control group with no history of COVID-19 (n=36), group 2 included those with mild to moderate pneumonia symptoms (n=43), and group 3 included those with severe pneumonia symptoms (n=29). The calcium scores were 23.25±36.8 in group 1, 27.65±33.4 in group 2, and 53.58±55.1 in group 3. The calcium score was found to be significantly higher in group 3 patients with severe pneumonia (group 1-2 p=0.885, group 1-3 p&#60;0.05, group 2-3 p&#60;0.05). <P> Conclusion: Although there is no conclusive evidence of a relationship between COVID-19 and atherosclerosis, our study suggests a possible relationship between them. Since this relationship was found especially in cases with severe disease in our study, we believe that the treatment should focus on preventing excessive inflammatory response, and such patients should be under control in terms of coronary artery disease.</P>]]></description> </item><item><title><![CDATA[Identifying Predictors for Hypoplastic Aortic Arch (HAA) in Pediatric Patients
with Complex Coarctation of the Aorta (CoA)]]></title><link>https://www.benthamscience.comarticle/139195</link><description><![CDATA[<p>Objective: HAA is a significant risk factor in complex CoA patients. We conducted a retrospective study to explore the relationship between HAA and other cardiovascular factors. <p> Methods: We analyzed 103 patients diagnosed with complex CoA using CT angiography and echocardiography. Aortic diameter was measured at six levels, and severe coarctation was defined as coarctation site to diaphragmatic level ratio (CDR) &#60; 50%. Correlations between non-HAA and HAA groups were assessed. Univariate and multivariate logistic regression identified HAA risk factors. <p> Results: Among 103 children with complex CoA, 55 were in the non-HAA group and 48 in the HAA group. The incidence of PDA (56.3% vs. 32.7%, p &#60; 0.05), severe coarctation (CDR &#60; 50%, 81.3% vs. 34.5%, p &#60; 0.01), and collateral arteries (39.6% vs. 0, p &#60; 0.01) were higher in the HAA group than one in the non-HAA group. The aortic arch size was positively correlated with age and negatively correlated with severe coarctation, VSD, collateral arteries, and left heart dysfunction. Logistic regression results showed that collateral arteries were risk factors for the whole aortic arch (proximal arch OR = 11.458; p &#60; 0.01, distal arch OR = 4.211; p &#60; 0.05, and isthmus OR = 11.744; p &#60; 0.01), severe coarctation (OR = 6.653; p &#60; 0.01), and left heart dysfunction (OR = 5.149; p &#60; 0.01) associated with isthmus hypoplasia. <p> Conclusion: This study highlights the prevalence of HAA in complex CoA patients and its associations with various cardiovascular factors. These insights improve diagnosis and treatment approaches.</p>]]></description> </item><item><title><![CDATA[Improving Women's Health and Immunity: A Thorough Mapping Micronutrients and Dietary Recommendations]]></title><link>https://www.benthamscience.comarticle/138610</link><description><![CDATA[In particular, throughout life, women's health depends on having an ideal micronutrient level. Thus, pregnancy outcomes and the long-term health of a woman's offspring are significantly influenced by her physical and nutritional well-being during the preconception stage. Various nutrients are required in sufficient amounts to fulfill the requirements at the various phases in the life of females. Our analysis of the state of nutrition shows illnesses connected to micronutrient deficiencies, particularly anemia and its related deficiencies. Peer-reviewed publication databases and publicly available data from international and national sources were targeted in a structured literature search to sort out the direct or indirect association between the different micronutrients, their levels, sources and significance in the various stages of life of females. The goal of the current review is to identify any direct or indirect relationships between the numerous micronutrients, their sources, concentrations, and importance at different phases of female development.]]></description> </item><item><title><![CDATA[Single-cell Technology in Stem Cell Research]]></title><link>https://www.benthamscience.comarticle/137519</link><description><![CDATA[Single-cell technology (SCT), which enables the examination of the fundamental units comprising biological organs, tissues, and cells, has emerged as a powerful tool, particularly in the field of biology, with a profound impact on stem cell research. This innovative technology opens new pathways for acquiring cell-specific data and gaining insights into the molecular pathways governing organ function and biology. SCT is not only frequently used to explore rare and diverse cell types, including stem cells, but it also unveils the intricacies of cellular diversity and dynamics. This perspective, crucial for advancing stem cell research, facilitates non-invasive analyses of molecular dynamics and cellular functions over time. Despite numerous investigations into potential stem cell therapies for genetic disorders, degenerative conditions, and severe injuries, the number of approved stem cell-based treatments remains limited. This limitation is attributed to the various heterogeneities present among stem cell sources, hindering their widespread clinical utilization. Furthermore, stem cell research is intimately connected with cutting-edge technologies, such as microfluidic organoids, CRISPR technology, and cell/tissue engineering. Each strategy developed to overcome the constraints of stem cell research has the potential to significantly impact advanced stem cell therapies. Drawing on the advantages and progress achieved through SCT-based approaches, this study aims to provide an overview of the advancements and concepts associated with the utilization of SCT in stem cell research and its related fields.]]></description> </item><item><title><![CDATA[Regenerative Medicine and Nanotechnology Approaches against Cardiovascular Diseases: Recent Advances and Future Prospective]]></title><link>https://www.benthamscience.comarticle/138387</link><description><![CDATA[Regenerative medicine refers to medical research focusing on repairing, replacing, or regenerating damaged or diseased tissues or organs. Cardiovascular disease (CVDs) is a significant health issue globally and is the leading cause of death in many countries. According to the Centers for Disease Control and Prevention (CDC), one person dies every 34 seconds in the United States from cardiovascular diseases, and according to a World Health Organization (WHO) report, cardiovascular diseases are the leading cause of death globally, taking an estimated 17.9 million lives each year. Many conventional treatments are available using different drugs for cardiovascular diseases, but these treatments are inadequate. Stem cells and nanotechnology are promising research areas for regenerative medicine treating CVDs. Regenerative medicines are a revolutionary strategy for advancing and successfully treating various diseases, intending to control cardiovascular disorders. This review is a comprehensive study of different treatment methods for cardiovascular diseases using different types of biomaterials as regenerative medicines, the importance of different stem cells in therapeutics, the expanded role of nanotechnology in treatment, the administration of several types of stem cells, their tracking, imaging, and the final observation of clinical trials on many different levels as well as it aims to keep readers up to pace on emerging therapeutic applications of some specific organs and disorders that may improve from regenerative medicine shortly.]]></description> </item><item><title><![CDATA[Unravelling the Impact: Pulmonary Side Effects of Anti-Seizure Medications]]></title><link>https://www.benthamscience.comarticle/138307</link><description><![CDATA[<p>Background: Epilepsy is a chronic brain condition affecting over 50 million people worldwide. Several new anti-seizure medications (ASMs) have been introduced to treat epilepsy in recent decades. </p> <p> Objective: Nearby the specific therapeutic action, ASMs, like other types of pharmacotherapy, can produce various side effects. In this review, we shall analyze the different pharmaceutical classes of ASMs, their mechanism of action, and their interaction with the respiratory system. </p> <p> Methods: This manuscript is based on a retrospective review of English publications indexed by Pubmed, UpToDate and datasheets published by the European Medicines Agency and the Food and Drug Administration (FDA), using various terms reminiscent of ASMs and pulmonary function. </p> <p> Results: ASMs act on organism homeostasis in different ways, acting on lung function directly and indirectly and playing a protective or damaging role. A damaging direct lung involvement ranged from infections, hypersensitivity reactions, and respiratory depression to other structured pulmonary diseases. Meanwhile, a damaging indirect effect, might be constituted by pulmonary artery hypertension. On the other hand, a protective effect might be the expression of developmental processing, decreasing airway remodelling in asthma patients, vascular remodelling in pulmonary hypertension and, nonetheless, anti-inflammatory and immunomodulatory actions. </p> <p> Conclusion: An adequate awareness of ASMs effects on the respiratory system seems essential for better managing frail individuals or/and those predisposed to respiratory disorders to improve our patients' clinical outcomes.</p>]]></description> </item><item><title><![CDATA[Diabetes and its Complications: Role of Luteolin, A Wonder Chemical from the Natural Source]]></title><link>https://www.benthamscience.comarticle/138879</link><description><![CDATA[Flavonoids have been reported to be vital in treating various chronic disorders. Luteolin (3′,4′,5,7-tetrahydroxyflavone) is a flavonoid present in a variety of plant sources such as celery, green pepper, olive oil, peppermint, thyme, rosemary, oregano, etc. It has been reported to have various pharmacological activities such as antioxidant, anti-inflammatory, anticancer, antidiabetic, anti-Alzheimer, antimicrobial, etc. Many scientific studies have been carried out on luteolin for its possible effects on diabetes and its associated complications. The present review focuses on the role of luteolin in diabetes mellitus and the associated complications. The antidiabetic impact of luteolin is linked with the increased expression of PPARγ and GLUT. Various in vitro and in vivo studies have been performed to explore the effects of luteolin on diabetic complications, and it has shown a significant impact in the management of the same.]]></description> </item><item><title><![CDATA[Cardioprotective Role of <i>Tinospora cordifolia</i> against Trimethylamine-N-Oxide and Glucose Induced Stress in Rat Cardiomyocytes]]></title><link>https://www.benthamscience.comarticle/135689</link><description><![CDATA[<p>Background: Type 2 diabetes has become a concern issue that affects the quality of life and can increase the risk of cardiac insufficiency elevating the threat to the life safety of patients. A recognized cause of cardiac insufficiency is diabetic cardiomyopathy, chronic hyperglycemia, and myocardial lipotoxicity which can reduce the myocardial contractile performance, and enhance the cardiomyocyte hypertrophy and interstitial fibrosis. The cause of diabetic cardiomyopathy is multi-factorial which includes oxidative stress, insulin resistance, inflammation, apoptosis, and autophagy. Recent clinical studies have suggested the dysbiosis of gut microbiota, secretion of metabolites, and their diffusion in to the host as to have direct detrimental effects on the cardiac contractility. </p> <p> Materials and Methods: In the present paper, we have done in silico studies including molecular interaction of phytoconstituents of <i>Tinospora cordifolia</i> against reactive oxygen species producing proteins. Whereas, in vitro studies were conducted on H9C2 cardiac cells including cell morphological examination, level of reactive oxygen species, cell count-viability, apoptotic status, in the presence of high glucose, trimethylamine-n-oxide, and plant extracts which were determined through cell analyzer and microscopic assays. </p> <p> Results: The treatment of high glucose and trimethylamine-n-oxide was found to be increase the cardiac stress approximately two fold by attenuating hypertrophic conditions, oxidative stress, and apoptosis in rat cardiomyocytes, and <i>Tinospora cordifolia</i> was found to be a cardioprotective agent. </p> <p> Conclusion: Conclusively, our study has reported that the Indian medicinal plant <i>Tinospora cordifolia</i> has the ability to treat diabetic cardiomyopathy. Our study can open up a new herbal therapeutic strategy against diabetic cardiomyopathy.</p>]]></description> </item><item><title><![CDATA[Therapeutic Potential of <i>Syzygium aromaticum</i> in Gut Dysbiosis <i>via</i> TMAO Associated Diabetic Cardiomyopathy]]></title><link>https://www.benthamscience.comarticle/133917</link><description><![CDATA[<p> Background: Dysbiosis of the gastrointestinal microbiota is not only related to the pathogenesis of intestinal disorders but also associated with extra-intestinal diseases. Various studies have revealed the role of an imbalance of intestinal microbiota and their metabolites including bile acids, indole derivatives, polyamines, and trimethylamine in the progression of various diseases. The elevated plasma level of the oxidized form of trimethylamine is associated with the increased risk of cardiovascular diseases. Literature supports that herbal medicines can modulate human health by altering the diversity of gut microbiota and their metabolites and proposes the use of prebiotics to improve dysbiotic conditions as a new way of therapeutic strategy. </p> <p> Methods: <i>In silico</i> studies including drug likeliness, toxicity prediction, and molecular interaction of phytochemicals against trimethylamine lyase enzyme have been done. Antimicrobial activity of extracts of selected plant i.e. <i>Syzygium aromaticum</i> was done by disc diffusion and the protective effects of plant compounds were examined on trimethylamine-n-oxide a bacterial metabolic product and high glucose induced toxicity. </p> <p> Results: The current study has found that the phytochemicals of <i>S. aromaticum</i> identified as nontoxic and followed the standard rules of drug likeliness and showed a significant binding affinity against trimethylamine-n-oxide producing enzymes. Furthermore, <i>S. aromaticum</i> extract was found to have antimicrobial potential and cardioprotective effects by reducing the production of intracellular reactive oxygen species and correcting the distorted nuclear morphology in the presence of high trimethylamine-n-oxide. </p> <p> Conclusion: Conclusively, our study explored the herbal intervention in intestinal dysbiosis and suggested a natural therapy against dysbiosis associated with cardiac disease, and <i>S, aromaticum</i> was found to have exceptional cardioprotective potential against TMAO induced gut dysbiosis, which provides a novel future therapeutic intervention for treating cardiovascular complications.</p>]]></description> </item><item><title><![CDATA[MicroRNAs Targeting Critical Molecular Pathways in Diabetic Cardiomyopathy Emerging Valuable for Therapy]]></title><link>https://www.benthamscience.comarticle/137695</link><description><![CDATA[MicroRNAs have emerged as an important regulator of post-transcriptional gene expression studied extensively in many cancers, fetal development, and cardiovascular diseases. Their endogenous nature and easy manipulation have made them potential diagnostic and therapeutic molecules. Diseases with complex pathophysiology such as Diabetic Cardiomyopathy display symptoms at a late stage when the risk of heart failure has become very high. Therefore, the utilization of microRNAs as a tool to study pathophysiology and device-sustainable treatments for DCM could be considered. The present review focuses on the mechanistic insights of diabetic cardiomyopathy and the potential role of microRNAs.]]></description> </item><item><title><![CDATA[Network Pharmacology and Bioinformatics Analyses Identify the Core Genes and Pyroptosis-Related Mechanisms of <i>Nardostachys Chinensis</i> for Atrial Fibrillation]]></title><link>https://www.benthamscience.comarticle/136961</link><description><![CDATA[<p> Background: <i>Nardostachys chinensis</i> is an herbal medicine widely used in the treatment of atrial fibrillation (AF), but the mechanism is unclear. <p> </p> Objective: To explore the molecular mechanism of <i>N. chinensis</i> against AF. <p> </p> Methods: The TCMSP was used to screen the active <i>N. chinensis</i> compounds and their targets. Differentially expressed genes (DEGs) for AF were identified using open-access databases. Using Venn diagrams, the cross-targets of <i>N. chinensis</i>, pyroptosis, and AF were obtained. The genes underwent molecular docking as well as gene set enrichment analysis (GSEA). A nomogram based on candidate genes was constructed and evaluated with the clinical impact curve. After that, the immune infiltration of the dataset was analyzed by single sample GSEA (ssGSEA). Finally, microRNAs (miRNAs) and transcription factors (TFs) were predicted based on candidate genes. <p> </p> Results: Tumor necrosis factor (TNF) and caspase-8 (CASP8) were obtained as candidate genes by taking the intersection of DEGs, targets of <i>N. chinensis</i>, and pyroptosis-related genes. Tolllike receptor (TLR) and peroxisome proliferator-activated receptor (PPAR) signaling pathways were linked to candidate genes. Additionally, immune cell infiltration analysis revealed that CASP8 was associated with natural killer T cells, natural killer cells, regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSC), macrophages, CD8 T cells, and CD4 T cells. Finally, miR-34a-5p and several TFs were found to regulate the expression of CASP8 and TNF. <p> </p>Conclusion: CASP8 and TNF are potential targets of <i>N. chinensis</i> intervention in pyroptosisrelated AF, and the TLR/NLRP3 signaling pathway may be associated with this process.</p>]]></description> </item><item><title><![CDATA[Regulation of ROS/inflammasome Axis is Essential for Cardiac Regeneration in Aging Rats Receiving Transplantation of Mesenchymal Stem Cells]]></title><link>https://www.benthamscience.comarticle/136351</link><description><![CDATA[<p>Background: Aging is a biological and gradual deterioration of function in living organisms. Aging is one of the risk factors for heart disease. </p> <p> Objective: Although mesenchymal stem cell transplantation shows potential in heart disease treatment, the relationship between stem cell-based therapy and oxidative stress/inflammasome axis regulation remains unclear. This study hypothesized that intervention of stem cells showed protective effect on heart aging induced by D-galactose through regulation of oxidative stress/inflammasome axis. </p> <p> Methods: An aging animal model was designed to test the above hypothesis. Experimental animals were divided into three groups, including Sham, D-gal (aging rats induced by d-galactose), and D-gal+WJSC (aging rats receiving mesenchymal stem cells). </p> <p> Results: Compared to the Sham, the experimental results indicate that structural alteration (HE stain and Masson’s Trichrome stain), oxidative stress elevation (increase of TBARS level, expression of gp-91 and suppression of Sirt-1 as well as SOD2), increase of aging marker p53, suppression of cardiogenesis marker Troponin T, and inflammasome related protein markers expression (NLRP3, caspase-1 and IL-1 beta) were significantly observed in D-gal. In contrast, all pathological pathways were significantly improved in D-gal+WJSC when compared to D-gal. In addition, migration of stem cells to aging heart tissues was observed in the D-gal+WJSC group. </p> <p> Conclusion: These findings suggest that mesenchymal stem cell transplantation effectively ameliorates aging hearts through oxidative stress/inflammasome axis regulation. The results from this study provide clinical potential for stem cell-based therapy in the treatment of aging hearts.</p>]]></description> </item><item><title><![CDATA[The Association between NADPH Oxidase 2 (NOX2) and Drug Resistance in Cancer]]></title><link>https://www.benthamscience.comarticle/138532</link><description><![CDATA[NADPH oxidase, as a major source of intracellular reactive oxygen species (ROS), assumes an important role in the immune response and oxidative stress response of the body. NADPH oxidase 2 (NOX2) is the first and most representative member of the NADPH oxidase family, and its effects on the development of tumor cells are gaining more and more attention. Our previous study suggested that NCF4 polymorphism in p40phox, a key subunit of NOX2, affected the outcome of diffuse large B-cell lymphoma patients treated with rituximab. It hypothesized that NOX2-mediated ROS could enhance the cytotoxic effects of some anti-tumor drugs in favor of patients with tumors. Several reviews have summarized the role of NOX2 and its congeners-mediated ROS in anti-tumor therapy, but few studies focused on the relationship between the expression of NOX2 and anti-tumor drug resistance. In this article, we systematically introduced the NOX family, represented by NOX2, and a classification of the latest inhibitors and agonists of NOX2. It will help researchers to have a more rational and objective understanding of the dual role of NOX2 in tumor drug resistance and is expected to provide new ideas for oncology treatment and overcoming drug resistance in cancer.]]></description> </item><item><title><![CDATA[Curcumin and Curcumin Derivatives for Therapeutic Applications:
<i>In vitro</i> and <i>In vivo</i> Studies]]></title><link>https://www.benthamscience.comarticle/137990</link><description><![CDATA[Curcumin is a naturally derived phytochemical compound obtained from the turmeric plant <i>Curcuma longa L.</i> (Zingiberaceae family), which is a popular spice and food color and has been actively researched for decades. It has been shown to have a variety of pharmacological properties both <i>in vitro</i> and <i>in vivo</i>. Several investigations have shown that curcumin's metabolites contribute to its pharmacological effectiveness. Curcumin has potent anti-inflammatory and anti-tumor activity when used alone or in conjunction with conventional treatments. There are various unique and diverse pharmacological effects of curcumin against various disease conditions like diabetes, inflammation, cancer, malaria, and Alzheimer's. The <i>in vitro</i> and <i>in vivo</i> mechanisms by which curcumin exerts its pharmacological effects are reviewed. Based on data from the clinical and experimental evaluation of curcumin in animal models and human subjects, the review summarizes the pharmacological effect of curcumin and its derivatives concerning anti-tumor property, their mechanism of action, and their cellular target. The current research focuses on identifying curcumin's function in the immune system's cascade and determining the ideal effective dose (ED50). Through <i>in-vitro</i> and <i>in-vivo</i> experiments, the current study aims to comprehend and establish the role of curcumin in the healing of disease conditions.]]></description> </item><item><title><![CDATA[A Systematic Review on the Potential Applications of Theranostic
Nanoparticles in Diabetes and its Associated Complication Diabetic
Neuropathy]]></title><link>https://www.benthamscience.comarticle/137581</link><description><![CDATA[<p>Background: Diabetes neuropathy is a frequent ailment that has a substantial impact on patients by increasing the risk of falls and causing discomfort. The lower extremities are where diabetic neuropathy patients first feel pain. This discomfort could seem like a pinprick, an electric shock, or something else. </p> <p> Objective: Here, we give a comprehensive overview of this quickly developing theranostic application that includes all relevant imaging, diagnostic, therapeutic, and monitoring elements for the management of diabetes and diabetes neuropathy. </p> <p> Methods: The data for the current study was gathered by searching PubMed and Google Scholar. Several research and review publications from various publishers, including Springer Nature, Bentham Science, PLOS one, MDPI, and ACS Publishing Centre, were evaluated to compile the data. </p> <p> Result: Recent developments in theranostics have shown promise as alternate management approaches for diabetes and ailments linked to diabetes. Numerous nanotechnology-built biosensors, including multiwalled carbon nanotubes, copper nanowires, zinc oxide tetrapods, and nanoparticle- embedded contact lenses, offer benefits in monitoring diabetic neuropathy. </p> <p> Conclusion: The potency, usability, and dependability of insulin substitutes have been demonstrated by a variety of innovative methods for the management of diabetes, which includes nanotechnology approaches using Gene-Based Nanoparticles (siRNA), Liposomes, Exosomes/ Extracellular Vesicles, Neuromodulation, and Inhalable Nanoparticles. Over the past few years, the development of various theranostic nanoparticles for Diabetic neuropathy has experienced an unprecedented expansion. Even though much work needs to be done to precisely evaluate the genuine benefits provided by these particles, such as issues with nanotoxicity, theranostic nanoparticles will have a significant impact on the field of nanomedicine.</p>]]></description> </item><item><title><![CDATA[Group 5 Pulmonary Hypertension: Multiple Systemic Diseases, Multiple
Mechanisms of Pulmonary Hypertension, and Multiple Management
Challenges]]></title><link>https://www.benthamscience.comarticle/138833</link><description><![CDATA[Group 5 pulmonary hypertension (PH) with unclear and/or multifactorial mechanisms includes a wide variety of conditions associated with PH, and the mechanisms by which PH develops vary dramatically depending on the underlying condition. Indeed, in many group 5 conditions, such as sarcoidosis, multiple distinct drivers of PH are present concurrently in a single patient, with the predominant factor depending on the predisposing disease phenotype. For this reason, thorough diagnostic evaluation to most accurately phenotype every patient with group 5 PH is essential. Treatment of these patients should begin by fully characterizing and optimizing the management of their underlying disease, often in conjunction with disease experts. Initial targets of PH treatment include identifying and correcting factors that worsen PH, such as volume overload and hypoxemia, as well as a complete PH evaluation, searching for other undiagnosed causes of PH (e.g., congenital heart disease or chronic thromboembolic disease). Data to guide treatment with therapies specific to pulmonary arterial hypertension (PAH) are inadequate for any specific recommendations, and adverse effects in group 5 patients are common. If these therapies are considered, evaluation by a multidisciplinary team that includes a PH specialist is recommended. Factors in the selection of PAH therapies should include consideration of the dominant physiologic features of the underlying disease, the severity of hemodynamic and right ventricular abnormalities, the risk of adverse drug effects, and any known contraindications to PAH-specific medications based on the underlying condition. Vigilant monitoring following initiation of PAH-specific therapy is critical, as the clinical effects are hard to predict, and untoward events, such as uncovering pulmonary veno-occlusive disease, may occur. Collaborative care by a multidisciplinary team of experts is key to the management of this challenging patient population.]]></description> </item><item><title><![CDATA[The Thyroid-cardiac Axis: Thyroid Function, Cardiac Rhythmology, and
Sudden Cardiac Death]]></title><link>https://www.benthamscience.comarticle/135865</link><description><![CDATA[It is well known that thyroid dysfunction increases the risk of cardiovascular mortality and morbidity. The pleiotropic effect of thyroid hormones has a profound effect on the cardiovascular system, influencing both the formation of a normal cardiac rhythm and rhythm disturbance. A number of research studies have demonstrated correlations between TSH and FT4 levels and significant cardiovascular events. The pathophysiological mechanisms underlying these complex associations are, however, inadequately defined. A system-based examination of the relationship between thyroid homeostasis and cardiovascular disease could pave the way for novel study areas and a more individualised strategy for the management of individuals at cardiovascular risk.]]></description> </item><item><title><![CDATA[Management of Pulmonary Hypertension during Pregnancy]]></title><link>https://www.benthamscience.comarticle/137469</link><description><![CDATA[Pregnancy in patients with pulmonary arterial hypertension (PAH) is a high-risk condition associated with high morbidity and mortality. Patients with severe PAH are often advised against pregnancy. Still, those patients who pursue pregnancy require a dedicated and multidisciplinary approach since the progression of fetal growth will accompany significant hemodynamic changes, which can be challenging for patients with a poorly functioning right ventricle. In this article, we describe the approach to the unique cardiovascular, respiratory, hematologic, and social challenges that pregnant patients with PAH face throughout pregnancy. We discuss the impact of these physiologic changes on diagnostic studies commonly used in PAH and how to incorporate diagnostic data in making the diagnosis and risk stratifying pregnant patients with PAH. The pharmacologic challenges of pulmonary vasodilators in pregnancy are discussed as well. Pregnant patients with PAH are at particularly high risk of mortality around the time of delivery, and we discuss the multidisciplinary approach to the management of these patients, including the use of anesthesia, inotropic support, type of delivery, and postpartum care, providing clinicians with a practical approach to the management of this difficult condition.]]></description> </item><item><title><![CDATA[Challenges in Genetic Diagnosis of Mitochondrial Diseases: What Can
Functional Genomics' Studies Do?]]></title><link>https://www.benthamscience.comarticle/136734</link><description><![CDATA[Introduction: Mitochondrial oxidative phosphorylation (OXPHOS) diseases are challenging both from clinical and therapeutic perspectives. The advent of next-generation sequencing (NGS) boosted the discovery of new genetic defects affecting OXPHOS, with pathogenic variants identified in >350 genes to date [1]. However, in many patients, novel variants of unknown clinical significance are found. Subsequent functional studies may clarify its pathogenic consequences and modify the variant’s classification, establishing a genetic diagnosis [2, 3]. <P> Methods: Analysis of data obtained from patients (P1-P5) with novel genetic causes and functional genomics’ studies performed, namely OXPHOS respiratory/glycolytic rates (Seahorse XF), enzymatic activity and assembly (BN-page), protein levels (SDS-WB), single muscle fiber assay, NGS and bioinformatics. <P> Results/Case Report: P1-Leigh syndrome (40y, male); Complex IV activity deficiency (full assembly absent), homozygous deletion (c.-11_13del, SURF1), not detected by NGS[2]. P2- Epileptic encephalopathy (8y, male); homozygous c.882-1G>A, FASTKD2; OXPHOS decrease; reduced FASTKD2 expression and abnormal respiratory/glycolytic rates. P3-Cardiomyopathy/ nephropathy (39y, male); c.29G>C, FASTKD2; OXPHOS decrease; reduced FASTKD2 levels. P4-CPEO (62y, female); multiple OXPHOS deficiency; mtDNA alterations (m.7486G>A, MTTS1; 4,977bp del); higher levels of mutant mtDNA alterations in COX-deficient fibers [3]. P5- Polyneuropathy (15y, female); heterozygous c.1437C>A, POLG; combined def. or normal OXPHOS activity/respiratory capacity (tissue variable), raised CI assembly; normal POLG levels. Also, proteins’ expression levels were reduced (P1-4), confirming pathogenicity. In P5, data do not support pathogenicity. <P> Conclusion: If specific functional results are similar to controls, one might inquire about the pathogenicity of the studied variant and more genetic or bioinformatics analyses and family investigations are needed. There are also limitations of NGS in mutation detection that Sanger sequencing can overcome (P1). When performed first, the OXPHOS activity may guide to genetic screening or interpretation, concordant to later assembly results. All cases were solved and data may be crucial for genetic counseling.]]></description> </item><item><title><![CDATA[Liraglutide Improves Diabetic Cardiomyopathy by Downregulation of
Cardiac Inflammatory and Apoptosis Markers]]></title><link>https://www.benthamscience.comarticle/136133</link><description><![CDATA[<p>Background: Diabetic cardiomyopathy is one of the leading causes of mortality for people with diabetes worldwide. The majority of the formalistic alterations in the heart associated with diabetic cardiomyopathy have been found to be primarily caused by the ongoing oxidative stress brought on by hyperglycemia, which leads to the dysfunctional reactions of apoptosis and inflammation. Liraglutide, a long-acting counterpart of glucagon-like peptide-1, has been demonstrated to have a number of therapeutic applications in medicine and other biological processes. </p> <p> Methods: The PubMed database was searched using the terms liraglutide, DCM, and all associated inflammatory markers. </p> <p> Results: There has been a lot of research on liraglutide's potential to protect the heart from cardiomyopathy brought on by diabetes. Liraglutide's therapeutic actions as an antioxidant, antihyperglycemic, anti-apoptotic, and anti-inflammatory medicine may help to lessen diabetic cardiomyopathy. </p> <p> Conclusion: The most recent studies on the effects of liraglutide therapy on DCM are presented in this review, along with an explanation of the underlying mechanisms.</p>]]></description> </item><item><title><![CDATA[Pulmonary Hypertension Related to Left Heart Disease (PH-LHD)]]></title><link>https://www.benthamscience.comarticle/140187</link><description><![CDATA[Pulmonary Hypertension secondary to left heart disease (PH-LHD) is the most common form of pulmonary hypertension (PH) and is a frequent complication of heart failure. It is associated with increased morbidity and mortality. The definitions of both PH and PH-LHD have changed over time and now generally follow those established by the 6th World Symposium on Pulmonary Hypertension (WSPH) in 2018 and the most recent European Society of Cardiology (ESC) guidelines in 2022. A systematic approach including clinical history and noninvasive testing is required to properly diagnose PH-LHD, and accurate hemodynamics by right heart catheterization, sometimes involving provocative testing, are often needed to diagnose PH-LHD but are essential to further subclassify PH-LHD into either isolated post-capillary pulmonary hypertension (Ipc-PH) <i>versus</i> combined pre and post-capillary pulmonary hypertension (Cpc-PH). This distinction is important as it guides therapeutic decisions and carries prognostic implications. Cpc-PH, in particular, shares some histo-pathologic and hemodynamic characteristics with pulmonary arterial hypertension (PAH) and, hence, the rationale for the potential use of pulmonary vasodilator therapy. To date, however, there is no strong evidence to support PAH-specific medications for Cpc- PH, and the mainstay of treatment for PH-LHD remains to treat the underlying cause of LHD. Further research is warranted to refine therapeutic approaches, improve long-term outcomes, and explore novel treatment modalities to alleviate the burden of PH in this patient population.]]></description> </item><item><title><![CDATA[Expression of Circulating miR-21 and -29 and their Association with
Myocardial Fibrosis in Hypertrophic Cardiomyopathy]]></title><link>https://www.benthamscience.comarticle/138201</link><description><![CDATA[<P>Background: Hypertrophic Cardiomyopathy (HCM) is characterized by myocardial hypertrophy, fibrosis, and sarcomeric disarray. <P> Objective: To evaluate the expression levels of circulating miR-21 and -29 in patients with HCM and their association with clinical characteristics and myocardial fibrosis. <P> Methods: In this case-control study, 27 subjects with HCM, 13 subjects with hypertensive cardiomyopathy, and 10 control subjects were enrolled. Evaluation of patients’ functional capacity was made by the six-minute walk test. Echocardiographic measurements of left ventricle systolic and diastolic function were conducted. Cardiac magnetic resonance late gadolinium enhancement (LGE) -through a semiquantitative evaluation- was used in the assessment of myocardial fibrosis extent in HCM patients. The expression of miR-21 and -29 in peripheral blood samples of all patients was measured via the method of quantitative reverse transcription polymerase chain reaction. <P> Results: Circulating levels of miR-21 were higher in both hypertensive and HCM (p<0.001) compared to controls, while expression of miR-29 did not differ between the three studied groups. In patients with HCM and LGE-detected myocardial fibrosis in more than 4 out of 17 myocardial segments, delta CT miR-21 values were lower than in patients with myocardial LGE in 3 or fewer myocardial segments (2.71 ± 1.06 deltaCT vs. 3.50 ± 0.55 deltaCT, p<0.04), indicating the higher expression of circulating miR-21 in patients with more extensive myocardial fibrosis. <P> Conclusion: MiR-21 was overexpressed in patients with HCM and hypertensive cardiomyopathy. Importantly, in patients with HCM, more extensive myocardial fibrosis was associated with higher levels of miR-21.</P>]]></description> </item><item><title><![CDATA[Recent Advances in the Treatment Strategies of Friedreich’s Ataxia: A Review
of Potential Drug Candidates and their Underlying Mechanisms]]></title><link>https://www.benthamscience.comarticle/139825</link><description><![CDATA[<P>Background: Friedreich's Ataxia (FRDA) is a rare hereditary neurodegenerative disorder characterized by progressive ataxia, cardiomyopathy, and diabetes. The disease is caused by a deficiency of frataxin, a mitochondrial protein involved in iron-sulfur cluster synthesis and iron metabolism. <P> Objective: This review aims to summarize recent advances in the development of treatment strategies for FRDA, with a focus on potential drug candidates and their mechanisms of action. <P> Methods: A comprehensive literature search was conducted using various authentic scientific databases to identify studies published in the last decade that investigated potential treatment strategies for FRDA. The search terms used included “Friedreich's ataxia”, “treatment”, “drug candidates”, and “mechanisms of action”. <P> Results: To date, only one drug got approval from US-FDA in the year 2023; however, significant developments were achieved in FRDA-related research focusing on diverse therapeutic interventions that could potentially alleviate the symptoms of this disease. Several promising drug candidates have been identified for the treatment of FRDA, which target various aspects of frataxin deficiency and aim to restore frataxin levels, reduce oxidative stress, and improve mitochondrial function. Clinical trials have shown varying degrees of success, with some drugs demonstrating significant improvements in neurological function and quality of life in FRDA patients. <P> Conclusion: While there has been significant progress in the development of treatment strategies for FRDA, further research is needed to optimize these approaches and identify the most effective and safe treatment options for patients. The integration of multiple therapeutic strategies may be necessary to achieve the best outcomes in FRDA management.</P>]]></description> </item><item><title><![CDATA[Relationship Between Vitamin D Level and Index of Cardio
Electrophysiological Balance in Children]]></title><link>https://www.benthamscience.comarticle/133663</link><description><![CDATA[<P>Background: Vitamin D deficiency has been found to be associated with various cardiovascular disorders, including hypertension, coronary artery disease, heart failure, peripheral vascular diseases, and sudden cardiac death. In the literature, it has been reported that many electrocardiographic parameters have been developed to predict ventricular arrhythmias. In recent studies, it is noteworthy that the index of cardio-electrophysiological balance (iCEB) and correct cardioelectrophysiological balance (iCEBc), which are electrocardiographic parameters, can be used as new, easy, cheap and non-invasive parameters to predict ventricular arrhythmias. <P> Objective: This study aimed to investigate the relationship between vitamin D deficiency and iCEB and iCEBc values in children. <P> Methods: A total of 186 patients were included in this study. Group 1 included 114 patients with vitamin D levels below 20 ng/ml; 50 patients with vitamin D levels of 21-29 ng/ml were included in Group 2; Group 3 consisted of 36 patients with a vitamin D level above 30 ng/ml. iCEB and iCEBc values were calculated by taking 12-lead ECG from all individuals and comparing them between groups. <P> Results: A total of 186 children, 114 subjects in Group 1, 36 subjects in Group 2, and 36 subjects in Group 3, were included in the study. Demographic characteristics and height-weight values of the groups were similar. Significant differences were found between the groups in terms of QT, QTc, QT/QRS, and QTc/QRS levels (p: 0.003, 0.028, 0.001, and 0.001, respectively). In the correlation analysis, a negative correlation was found between QTc/QRS and vitamin D level (r=-0.320, p=<0.001) and between QT/QRS and vitamin D level (r=-0.268, p=<0.001). Moreover, vitamin D level (&#946;=0.389, p<0.001) was determined as an independent predictor of QTc/QRS in multivariate logistic regression analysis. <P> Conclusion: iCEB and iCEBc parameters increase significantly in children with low vitamin D levels. These parameters are also evaluated during the follow-up of children with vitamin D deficiency in terms of the risk of ventricular arrhythmia. iCEBc can be used as an easy, inexpensive, non-invasive, and reproducible parameter.</P>]]></description> </item><item><title><![CDATA[Arrhythmias and Hypertrophic Cardiomyopathy: Unravelling the
Connection]]></title><link>https://www.benthamscience.comarticle/137835</link><description><![CDATA[Hypertrophic cardiomyopathy (HCM) results from gene mutations affecting cardiac sarcomeres and is inherited in an autosomal dominant manner. With a prevalence of 1:200-1:500 in the general population, HCM is characterised by a hypertrophied and non-dilated left ventricle with predominant involvement of the interventricular septum. The myocardium's structural and intracellular factors, combined with triggers such as physical exertion, autonomic dysfunction, and ischemia, can lead to reentry events, and atrial and ventricular arrhythmias, including atrial fibrillation (AF) which is common among HCM patients. To manage the increased risk of mortality arising from congestive heart failure and thromboembolism, in patients with AF long-term anticoagulation and antiarrhythmic drugs are employed. HCM patients may also encounter supraventricular and ventricular arrhythmias, such as nonsustained ventricular tachycardia and ventricular premature beats, which can potentially lead to sudden cardiac death and necessitate treatment with implanted defibrillators. Physicians must comprehensively analyse clinical, anatomical, hemodynamic, rhythmic, functional, and genetic characteristics to identify HCM patients at high risk of sudden death. This article aims to discuss the pathophysiology of arrhythmia in HCM and clinical recommendations for various ventricular and atrial fibrillation including catheter ablation and implantable cardioverter-defibrillator (ICD).]]></description> </item><item><title><![CDATA[Diabetic Retinopathy Leading to Blindness- A Review]]></title><link>https://www.benthamscience.comarticle/137696</link><description><![CDATA[Diabetic retinopathy (DR) is the most common microvascular complication of diabetes that damages the retina, leading to blindness. People with type 1 diabetes are at greater risk of developing DR than people with type 2 diabetes. Diabetic retinopathy may be divided into two primary categories: Proliferative diabetic retinopathy (PDR) and non-proliferative diabetic retinopathy (NPDR). There are multiple risk factors for the onset and progression of diabetic retinopathy, such as hypertension, obesity, smoking, duration of diabetes, and genetics. Numerous investigations have evaluated the levels of a wide range of inflammatory chemokines within DR patients' serum, vitreous, and aqueous fluids. In diabetic retinopathy, the vitreous fluid exhibited rises in angiogenic factors like platelet-derived growth factor (PDGF) or vascular endothelial growth factor (VEGF) or declines in antiangiogenic factors like pigment epithelium-derived factor (PEDF). For prevention of diabetic retinopathy, more physical activity as well as less sedentary behavior were linked to a reduced likelihood of DR. Supplementing with nutraceuticals containing vitamins (B1, B2, B6, B12, C, D, E, and l-methyl folate) and mineral (zinc) can help decrease or avoid an outbreak of DR. Only laser photocoagulation and Anti-vascular endothelial growth factor (Anti-VEGF) injections are advised as favorable therapies in severe retinopathy. When it comes to treating DR's VEGF levels, inflammation, oxidative stress, apoptosis, and angiogenesis, Traditional Chinese medicine (TCM) has an excellent future.]]></description> </item><item><title><![CDATA[Microfluidics-mediated Liposomal Nanoparticles for Cancer Therapy:
Recent Developments on Advanced Devices and Technologies]]></title><link>https://www.benthamscience.comarticle/138854</link><description><![CDATA[Liposomes, spherical particles with phospholipid double layers, have been extensively studied over the years as a means of drug administration. Conventional manufacturing techniques like thin-film hydration and extrusion have limitations in controlling liposome size and distribution. Microfluidics enables superior tuning of parameters during the self-assembly of liposomes, producing uniform populations. This review summarizes microfluidic methods for engineering liposomes, including hydrodynamic flow focusing, jetting, micro mixing, and double emulsions. The precise control over size and lamellarity afforded by microfluidics has advantages for cancer therapy. Liposomes created through microfluidics and designed to encapsulate chemotherapy drugs have exhibited several advantageous properties in cancer treatment. They showcase enhanced permeability and retention effects, allowing them to accumulate specifically in tumor tissues passively. This passive targeting of tumors results in improved drug delivery and efficacy while reducing systemic toxicity. Promising results have been observed in pancreatic, lung, breast, and ovarian cancer models, making them a potential breakthrough in cancer therapy. Surface-modified liposomes, like antibodies or carbohydrates, also achieve active targeting. Overall, microfluidic fabrication improves reproducibility and scalability compared to traditional methods while maintaining drug loading and biological efficacy. Microfluidics-engineered liposomal formulations hold significant potential to overcome challenges in nanomedicine-based cancer treatment.]]></description> </item><item><title><![CDATA[An Updated Review on the Significance of DNA and Protein
Methyltransferases and De-methylases in Human Diseases: From
Molecular Mechanism to Novel Therapeutic Approaches]]></title><link>https://www.benthamscience.comarticle/132369</link><description><![CDATA[Epigenetic mechanisms are crucial in regulating gene expression. These mechanisms include DNA methylation and histone modifications, like methylation, acetylation, and phosphorylation. DNA methylation is associated with gene expression suppression; however, histone methylation can stimulate or repress gene expression depending on the methylation pattern of lysine or arginine residues on histones. These modifications are key factors in mediating the environmental effect on gene expression regulation. Therefore, their aberrant activity is associated with the development of various diseases. The current study aimed to review the significance of DNA and histone methyltransferases and demethylases in developing various conditions, like cardiovascular diseases, myopathies, diabetes, obesity, osteoporosis, cancer, aging, and central nervous system conditions. A better understanding of the epigenetic roles in developing diseases can pave the way for developing novel therapeutic approaches for affected patients.]]></description> </item><item><title><![CDATA[Progress in Cardiac Magnetic Resonance Feature Tracking for Evaluating
Myocardial Strain in Type-2 Diabetes Mellitus]]></title><link>https://www.benthamscience.comarticle/137384</link><description><![CDATA[The global prevalence of type-2 diabetes mellitus (T2DM) has caused harm to human health and economies. Cardiovascular disease is one main cause of T2DM mortality. Increased prevalence of diabetes and associated heart failure (HF) is common in older populations, so accurately evaluating heart-related injury and T2DM risk factors and conducting early intervention are important. Quantitative cardiovascular system imaging assessments, including functional imaging during cardiovascular disease treatment, are also important. The left-ventricular ejection fraction (LVEF) has been traditionally used to monitor cardiac function; it is often preserved or increased in early T2DM, but subclinical heart deformation and dysfunction can occur. Myocardial strains are sensitive to global and regional heart dysfunction in subclinical T2DM. Cardiac magnetic resonance feature-tracking technology (CMR-FT) can visualize and quantify strain and identify subclinical myocardial injury for early management, especially with preserved LVEF. Meanwhile, CMR-FT can be used to evaluate the multiple cardiac chambers involvement mediated by T2DM and the coexistence of complications. This review discusses CMR-FT principles, clinical applications, and research progress in the evaluation of myocardial strain in T2DM.]]></description> </item><item><title><![CDATA[Current Landscape of Gene Therapy for the Treatment of Cardiovascular
Disorders]]></title><link>https://www.benthamscience.comarticle/138068</link><description><![CDATA[Cardiovascular disorders (CVD) are the primary cause of death worldwide. Multiple factors have been accepted to cause cardiovascular diseases; among them, smoking, physical inactivity, unhealthy eating habits, age, and family history are flag-bearers. Individuals at risk of developing CVD are suggested to make drastic habitual changes as the primary intervention to prevent CVD; however, over time, the disease is bound to worsen. This is when secondary interventions come into play, including antihypertensive, anti-lipidemic, anti-anginal, and inotropic drugs. These drugs usually undergo surgical intervention in patients with a much higher risk of heart failure. These therapeutic agents increase the survival rate, decrease the severity of symptoms and the discomfort that comes with them, and increase the overall quality of life. However, most individuals succumb to this disease. None of these treatments address the molecular mechanism of the disease and hence are unable to halt the pathological worsening of the disease. Gene therapy offers a more efficient, potent, and important novel approach to counter the disease, as it has the potential to permanently eradicate the disease from the patients and even in the upcoming generations. However, this therapy is associated with significant risks and ethical considerations that pose noteworthy resistance. In this review, we discuss various methods of gene therapy for cardiovascular disorders and address the ethical conundrum surrounding it.]]></description> </item><item><title><![CDATA[Chemistry, Biological Properties, and Bio-analysis of Tafamidis, a New
Transthyretin Stabilizer: A Systematic Review]]></title><link>https://www.benthamscience.comarticle/136411</link><description><![CDATA[<p>Background: Cardiomyopathy is a global health crisis that affects people all over the world. Consequently, scientists felt compelled to look for and develop ever-more-powerful pharmaceuticals. For ATTR-CM, the only drug currently recommended by the European Society of Cardiology is Tafamidis. <p> Objectives: The primary aim of this review article is to understand the chemistry, pharmacodynamic, pharmacokinetic, and bio-analytical methods available for Tafamidis. <p> Methods: A systematic review of the existing resources was accomplished up to 2022, comprising existing studies forming the database covering the existing resources from Web of Science, ScienceDirect, and PubMed. <p> Results: The review was based on a systematic review of all the existing studies used to formulate the database. The study also illustrated the PRISMA design that systematically analyses the prevalent resources. <p> Conclusion: Minimal analytical techniques are observed for quantifying the Tafamidis and transthyretin kinetic stabiliser. Therapeutic, pharmacological, and analytical considerations for the novel drug Tafamidis are discussed in this review. Particular attention is paid to the many different analytical and bioanalytical methods currently available for estimating Tafamidis, and the need is highlighted to develop a straightforward, validated technique that meets green chemistry standards.</p>]]></description> </item><item><title><![CDATA[Autophagy Behavior under Local Hypothermia in Myocardiocytes Injury]]></title><link>https://www.benthamscience.comarticle/133348</link><description><![CDATA[Hypothermia and autophagy are critical regulators of cell homeostasis by regulating intra and intercellular cell communication. Myocardiocyte cryotherapy poses multiple cellular and subcellular effects on the injured cell, including upregulation of autophagy. Autophagy plays a crucial role in modifying cell metabolism by regulating downregulation, reducing reactive oxygen species production, and improving the natural cellular antioxidant defense system. Reduction of reactive oxygen species production and improving natural cellular antioxidant defense system. Therapeutic hypothermia ranges from 32-34°C in terms of local myocardiocyte cooling. Hypothermia induces autophagy by phosphorylating the Akt signaling pathway. Hypothermia has a more therapeutic effect when applied at the beginning of reperfusion rather than in the beginning of ischemia. Moderate hypothermia with 33°C poses most therapeutic effect by viability maintaining and reduction of reactive oxygen species release. Application of local hypothermia to myocardiocytes can be applied to infarcted myocardiocytes, anginal and to the cardiomyopathies.]]></description> </item><item><title><![CDATA[Why have SGLT2 Inhibitors Failed to Achieve the Desired Success in
COVID-19?]]></title><link>https://www.benthamscience.comarticle/139495</link><description><![CDATA[The SARS-CoV-2 virus emerged towards the end of 2019 and caused a major worldwide pandemic lasting at least 2 years, causing a disease called COVID-19. SARS-CoV-2 caused a severe infection with direct cellular toxicity, stimulation of cytokine release, increased oxidative stress, disruption of endothelial structure, and thromboinflammation, as well as angiotensin-converting enzyme 2 (ACE2) down-regulation-mediated renin-angiotensin system (RAS) activation. In addition to glucosuria and natriuresis, sodium-glucose transport protein 2 (SGLT2) inhibitors (SGLT2i) cause weight loss, a decrease in glucose levels with an insulin-independent mechanism, an increase in erythropoietin levels and erythropoiesis, an increase in autophagy and lysosomal degradation, Na<sup>+</sup>/H<sup>+</sup>-changer inhibition, prevention of ischemia/reperfusion injury, oxidative stress and they have many positive effects such as reducing inflammation and improving vascular function. There was great anticipation for SGLT2i in treating patients with diabetes with COVID-19, but current data suggest they are not very effective. Moreover, there has been great confusion in the literature about the effects of SGLT2i on COVID-19 patients with diabetes . Various factors, including increased SGLT1 activity, lack of angiotensin receptor blocker co-administration, the potential for ketoacidosis, kidney injury, and disruptions in fluid and electrolyte levels, may have hindered SGLT2i's effectiveness against COVID-19. In addition, the duration of use of SGLT2i and their impact on erythropoiesis, blood viscosity, cholesterol levels, and vitamin D levels may also have played a role in their failure to treat the virus. This article aims to uncover the reasons for the confusion in the literature and to unravel why SGLT2i failed to succeed in COVID-19 based on some solid evidence as well as speculative and personal perspectives.]]></description> </item><item><title><![CDATA[Hydrogen Sulfide: Physiological Roles and Therapeutic Implications
against COVID-19]]></title><link>https://www.benthamscience.comarticle/131379</link><description><![CDATA[The COVID-19 pandemic due to severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) poses a major menace to economic and public health worldwide. Angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) are two host proteins that play an essential function in the entry of SARS-- COV-2 into host cells. Hydrogen sulfide (H<sub>2</sub>S), a new gasotransmitter, has been shown to protect the lungs from potential damage through its anti-inflammatory, antioxidant, antiviral, and anti-aging effects. It is well known that H<sub>2</sub>S is crucial in controlling the inflammatory reaction and the pro-inflammatory cytokine storm. Therefore, it has been suggested that some H<sub>2</sub>S donors may help treat acute lung inflammation. Furthermore, recent research illuminates a number of mechanisms of action that may explain the antiviral properties of H<sub>2</sub>S. Some early clinical findings indicate a negative correlation between endogenous H<sub>2</sub>S concentrations and COVID-19 intensity. Therefore, reusing H<sub>2</sub>S-releasing drugs could represent a curative option for COVID-19 therapy.]]></description> </item><item><title><![CDATA[Nicotinamide Mononucleotide in the Context of Myocardiocyte Longevity]]></title><link>https://www.benthamscience.comarticle/136793</link><description><![CDATA[Cellular and subcellular metabolic activities are crucial processes involved in the regulation of intracellular homeostasis, including cellular and subcellular signaling pathways. Dysregulation of intracellular regulation mechanisms is catastrophic and cumulates into cell death. To overcome the issue of dysregulation of intracellular regulation mechanisms, the preservation of subcellular and extracellular components is essential to maintain healthy cells with increased longevity. Several physiopathological changes occur during cell ageing, one of which is the dysregulation of intracellular physiology of the oxidative phosphorylation process. Nicotinamide mononucleotide (NMN) remains in the debut of anti-aging therapeutic effect. Aged myocardiocyte characterized by disrupted NMN and or its precursors or signaling pathways. Simultaneously, several other pathophysiological occur that collectively impair intracellular homeostasis. The NMN role in the antiaging effect remains unclear and several hypotheses have been introduced into describing the mechanism and the potential outcomes from NMN exogenous supply. Correction of the impaired intracellular homeostasis includes correction to the NMN metabolism. Additionally, autophagy correction, which is the key element in the regulation of intracellular intoxication, including oxidative stress, unfolding protein response, and other degradation of intracellular metabolites. Several signaling pathways are involved in the regulation mechanism of NMN effects on myocardiocyte health and further longevity. NMN protects myocardiocytes from ischemic injury by reducing anabolism and, increasing catabolism and further passing the myocardiocytes into dormant status. NMN applications include ischemic heart, disease, and failed heart, as well as dilated cardiomyopathies. Cytosolic and mitochondrial NADPH are independently functioning and regulating. Each of these plays a role in the determination of the longevity of the myocardiocytes. NMN has a cornerstone in the functionality of Sirtuins, which are an essential anti-senescent intrinsic molecule. The study aims to assess the role of NMN in the longevity and antisenescent of myocardiocytes.]]></description> </item><item><title><![CDATA[N-Stearoylethanolamine Exerts Cardioprotective Effects in Old Rats]]></title><link>https://www.benthamscience.comarticle/137879</link><description><![CDATA[<p>Background: Aging is associated with the slowing down of metabolic processes, diminished physiological processes, changes in hormonal activity and increasing exposure to oxidative stress factors and chronic inflammation. The endocannabinoid system (ECS) is a major signaling network that plays a pro-homeostatic role in the central and peripheral organs of the human body. A class of minor lipids, N-acylethanolamines (NAEs), which do not activate cannabinoid receptors, except for anandamide, but can potentiate the action of endocannabinoids and have a wide spectrum of biological activity and significant adaptogenic potential, belongs to ECS. The results of different studies over the past decades have established the protective effect of NAE on many pathological conditions. <p> Objective: This study aimed to investigate the cardioprotective effects of C18:0 NAE— N-stearoylethanolamine (NSE) in aged rats. In this study, we focused on investigating the effects of C18:0 NAE— N-stearoylethanolamine (NSE) on the intensity of oxidative/ nitrosative stress, antioxidant potential, lipoprotein profile and inflammation markers of blood plasma, phospholipid composition and age-related morphological changes of old rat heart tissues. <p> Methods: The study was conducted on Sprague Dawley male laboratory rats. The three groups of rats were involved in the study design. The first group consisted of young rats aged 4 months (n=10). The second (n=10) and third (n=10) groups included old rats aged of 18 months. Rats from the third group were administered a per os aqueous suspension of NSE at a dose of 50 mg/kg of body weight daily for 10 days. All groups of rats were kept on a standard vivarium diet. The blood plasma, serum, and heart of rats were used for biochemical and histological analysis. <p> Results: The cardioprotective effect of N-stearoylethanolamine in old rats was established, which was expressed in the normalization of the antioxidant system condition and the level of proinflammatory cytokines, positive modulation of blood plasma and lipoprotein profile, normalization of heart tissue lipid composition, and significant reduction in age-related myocardium morphological changes. <p> Conclusion: The revealed effects of N-stearoylethanolamine can become the basis for developing a new drug for use in complex therapy to improve the quality of life of older people.</p>]]></description> </item><item><title><![CDATA[Zamzam Water Mitigates Cardiac Toxicity Risk through Modulation of GUT
Microbiota and the Renin-angiotensin System]]></title><link>https://www.benthamscience.comarticle/139447</link><description><![CDATA[<p>Background: Cardiovascular diseases (CVDs) continue to exert a substantial global influence in specific areas due to population growth, aging, microbiota, and genetic/environmental factors. Drinking water has a strong impact on the health of an individual. Further, emerging evidence has highlighted the therapeutic potential and benefits of Zamzam water (Zam). <p> Objective: We investigated the influence of Zam on doxorubicin-induced cardiac toxicity, elucidating its consequential effects on GUT microbiota dysbiosis and hepatic and renal functions. <p> Methods: Male rats were categorized into four groups: Group 1 as Normal control (NC), Group 2 as Zamzam control (ZC), Group 3 Disease control (DC) and Group 4 as Therapeutic control (DZ) treated with Zam against doxorubicin-induced disease at a dose of 1mg/kg boy weight) intraperitoneally (i.p). <p> Results: Significant dysbiosis in the composition of GM was observed in the DC group along with a significant decrease (p &#60; 0.05) in serum levels of Zinc, interleukin-10 (IL-10), IL-6 and Angiotensin II (Ang II), while C-reactive protein (CRP), fibrinogen, and CKMB increased significantly (restoration of Zinc ions (0.72 ± 0.07 mcg/mL) compared to NC. Treatment with Zamzam exhibited a marked abundance of 18-times to 72% in Romboutsia, a genus of firmicutes, along with lowering of Proteobacteria in DZ followed by significant restoration of Zinc ions (0.72 ± 0.07 mcg/mL), significant (p ˂ 0.05) reduction in CRP (7.22 ± 0.39 mg/dL), CKMB (118.8 ± 1.02 U/L) and Fibrinogen (3.18 ± 0.16 mg/dL), significant (p &#60; 0.05) increase in IL-10 (7.22 ± 0.84 pg/mL) and IL-6 (7.18 ± 0.40 pg/ml), restoration of Ang II (18.62 ± 0.50 nmol/mL/min), marked increase in renin with normal myocyte architecture and tissue orientation of kidney, and restoration of histological architecture of hepatocyte. <p> Conclusion: Zam treatment mitigated cardiac toxicity risk through the modulation of GUT microbiota and the renin-angiotensin system and tissue histology effectively.</p>]]></description> </item><item><title><![CDATA[Network Pharmacology along with Molecular Docking to Explore the Mechanism of
Danshen Injection against Anthracycline-induced Cardiotoxicity and Transcriptome
Validation]]></title><link>https://www.benthamscience.comarticle/139149</link><description><![CDATA[<p>Introduction: Although anthracyclines have demonstrated efficacy in cancer therapy, their utilization is constrained by cardiotoxicity. In contrast, Danshen injection (DSI), derived from Salvia miltiorrhiza, has a longstanding tradition of being employed to ameliorate cardiovascular ailments, including anthracycline- induced cardiotoxicity (AIC). Nonetheless, there is a notable dearth of comprehensive systematic investigation into the molecular mechanisms underlying DSI's effects on AIC. Consequently, this study was undertaken to explore the underlying mechanism by which DSI acted against AIC. <p> Methods: Employing network pharmacology approach, the current investigation undertook a comprehensive analysis of the impact of DSI on AIC, which was further validated by transcriptome sequencing with <i>in vitro</i> AIC model. Additionally, molecular docking was conducted to evaluate the binding of active ingredients to core targets. A total of 3,404 AIC-related targets and 12 active ingredients in DSI, including chrysophanol, luteolin, tanshinone IIA, isoimperatorin, among others, were collected by differentially expressed analysis and database search, respectively. <p> Results: The network pharmacology and enrichment analysis suggested 102 potential targets and 29 signaling pathways associated with the protective effect of DSI on AIC. Three core targets (CA12, NOS3, and POLH) and calcium signaling pathways were further validated by transcriptomic analysis of the <i>in-vitro</i> model. The high affinity of the active ingredients binding to corresponding targets was confirmed by molecular docking. <p> Conclusion: The present study suggested that DSI might exert a cardioprotective effect on AIC via the inhibition of CA12, NOS3, and POLH, as well as the modulation of calcium signaling. Further experiments are warranted to verify the findings.</p>]]></description> </item><item><title><![CDATA[Cellular and Mitochondrial Pathways Contribute to SGLT2
Inhibitors-mediated Tissue Protection: Experimental and Clinical Data]]></title><link>https://www.benthamscience.comarticle/139413</link><description><![CDATA[In metabolic syndrome and diabetes, compromised mitochondrial function emerges as a critical driver of cardiovascular disease, fueling its development and persistence, culminating in cardiac remodeling and adverse events. In this context, angiotensin II - the main interlocutor of the renin-angiotensin-aldosterone system - promotes local and systemic oxidative inflammatory processes. To highlight, the low activity/expression of proteins called sirtuins negatively participates in these processes, allowing more significant oxidative imbalance, which impacts cellular and tissue responses, causing tissue damage, inflammation, and cardiac and vascular remodeling. The reduction in energy production of mitochondria has been widely described as a significant element in all types of metabolic disorders. Additionally, high sirtuin levels and AMPK signaling stimulate hypoxia- inducible factor 1 beta and promote ketonemia. Consequently, enhanced autophagy and mitophagy advance through cardiac cells, sweeping away debris and silencing the orchestra of oxidative stress and inflammation, ultimately protecting vulnerable tissue from damage. To highlight and of particular interest, SGLT2 inhibitors (SGLT2i) profoundly influence all these mechanisms. Randomized clinical trials have evidenced a compelling picture of SGLT2i emerging as game-changers, wielding their power to demonstrably improve cardiac function and slash the rates of cardiovascular and renal events. Furthermore, driven by recent evidence, SGLT2i emerge as cellular supermolecules, exerting their beneficial actions to increase mitochondrial efficiency, alleviate oxidative stress, and curb severe inflammation. Its actions strengthen tissues and create a resilient defense against disease. In conclusion, like a treasure chest brimming with untold riches, the influence of SGLT2i on mitochondrial function holds untold potential for cardiovascular health. Unlocking these secrets, like a map guiding adventurers to hidden riches, promises to pave the way for even more potent therapeutic strategies.]]></description> </item><item><title><![CDATA[Pharmacological Triggers of Takotsubo Cardiomyopathy: An Updated
Review of Evidence and Recommendations]]></title><link>https://www.benthamscience.comarticle/138278</link><description><![CDATA[<p>Background: Previous publications in 2011, 2016, and 2022 have presented lists of drugs associated with takotsubo cardiomyopathy (TCM). This review aims to provide updated drug lists that have been reported as potential causes of TCM. <p> Methods: Following the same methodology employed in previous reviews, a detailed investigation was carried out in the PubMed/Medline database from June 2022 to July 2023 to identify drug-induced TCM (DITC) case reports. Various search terms related to the drug-induced transient left ventricular ballooning syndrome, ampulla cardiomyopathy, apical ballooning syndrome, drug-induced broken heart syndrome, drug triggered takotsubo cardiomyopathy, takotsubo cardiomyopathy, and iatrogenic takotsubo cardiomyopathy were utilized. Filters for fulltext availability, case reports, human studies, and English language were applied. Articles reporting drugs associated with TCM development were included in the analysis. <p> Results: Foremost 192 case reports were initially identified, with 75 drugs meeting the inclusion criteria after a thorough review. The latest revision identified seven drugs that might lead to TCM, with four drugs (57.14%) already reported in previous reviews and three drugs (42.86%) newly identified. Consequently, the updated drug list potentially triggering TCM in 2023 comprises a sum of 75 drugs. <p> Conclusion: The recent 75 drugs provided additional evidence linking to TCM development. The updated list predominantly includes drugs that induce sympathetic overstimulation, although some drugs on the list have unclear associations with sympathetic nervous system activation.</p>]]></description> </item><item><title><![CDATA[Cardiac Amyloidosis: A Contemporary Review of Medical and Surgical
Therapy]]></title><link>https://www.benthamscience.comarticle/134823</link><description><![CDATA[Amyloidosis is a systemic disease initiated by deposition of misfolded proteins in the extracellular space, due to which multiple organs may be affected concomitantly. Cardiac amyloidosis, however, remains a major cause of morbidity and mortality in this population due to infiltrative /restrictive cardiomyopathy. This review attempts to focus on contemporary medical and surgical therapies for the different types of cardiac amyloidosis. Amyloidosis affecting the heart are predominantly of the transthyretin type (acquired in the older or genetic in the younger patients), and the monoclonal immunoglobulin light chain (AL) type which is solely acquired. A rare form of secondary amyloidosis AA type can also affect the heart due to excessive production and accumulation of the acute-phase protein called Serum Amyloid A” (SAA) in the setting of chronic inflammation, cancers or autoinflammatory disease. More commonly AA amyloidosis is seen in the liver and kidney. Other rare types are Apo A1 and Isolated Atrial Amyloidosis (AANF). Medical therapies have made important strides in the clinical management of the two common types of cardiac amyloidosis. Surgical therapies such as mechanical circulatory support and cardiac transplantation should be considered in appropriate patients. Future research using AI driven algorithms for early diagnosis and treatment as well as development of newer genetic engineering technologies will drive improvements in diagnosis, treatment and patient outcomes.]]></description> </item><item><title><![CDATA[The Golden Spice for Life: Turmeric with the Pharmacological Benefits of Curcuminoids Components, Including Curcumin, Bisdemethoxycurcumin, and Demethoxycurcumins]]></title><link>https://www.benthamscience.comarticle/132370</link><description><![CDATA[<p> Background: Turmeric (<i>Curcuma longa</i> L.), belonging to the Zingiberaceae family, is a perennial rhizomatous plant of tropical and subtropical regions. The three major chemical components responsible for the biological activities of turmeric are curcumin, demethoxycurcumin, and bisdemethoxycurcumin. </p><p> Methods: The literature search included review articles, analytical studies, randomized control experiments, and observations, which have been gathered from various sources, such as Scopus, Google Scholar, PubMed, and ScienceDirect. A review of the literature was carried out using the keywords: turmeric, traditional Chinese medicine, traditional Iranian medicine, traditional Indian medicine, curcumin, curcuminoids, pharmaceutical benefits, turmerone, demethoxycurcumin, and bisdemethoxycurcumin. The main components of the rhizome of the leaf are α-turmerone, β-turmerone, and arturmerone. </p><p> Results: The notable health benefits of turmeric are antioxidant activity, gastrointestinal effects, anticancer effects, cardiovascular and antidiabetic effects, antimicrobial activity, photoprotector activity, hepatoprotective and renoprotective effects, and appropriate for the treatment of Alzheimer's disease and inflammatory and edematic disorders. </p><p> Discussion: Curcuminoids are phenolic compounds usually used as pigment spices with many health benefits, such as antiviral, antitumour, anti-HIV, anti-inflammatory, antiparasitic, anticancer, and antifungal effects. Curcumin, bisdemethoxycurcumin, and demethoxycurcumin are the major active and stable bioactive constituents of curcuminoids. Curcumin, which is a hydroponic polyphenol, and the main coloring agent in the rhizomes of turmeric, has anti-inflammatory, antioxidant, anti-cancer, and anticarcinogenic activities, as well as beneficial effects for infectious diseases and Alzheimer's disease. Bisdemethoxycurcumin possesses antioxidant, anti-cancer, and anti-metastasis activities. Demethoxycurcumin, which is another major component, has anti-inflammatory, antiproliferative, and anti-cancer activities and is the appropriate candidate for the treatment of Alzheimer's disease. </p><p> Conclusion: The goal of this review is to highlight the health benefits of turmeric in both traditional and modern pharmaceutical sciences by considering the important roles of curcuminoids and other major chemical constituents of turmeric.</p>]]></description> </item><item><title><![CDATA[Biology of Tenascin C and its Role in Physiology and Pathology]]></title><link>https://www.benthamscience.comarticle/130686</link><description><![CDATA[Tenascin-C (TNC) is a multimodular extracellular matrix (ECM) protein hexameric with several molecular forms (180-250 kDa) produced by alternative splicing at the pre-mRNA level and protein modifications. The molecular phylogeny indicates that the amino acid sequence of TNC is a well-conserved protein among vertebrates. TNC has binding partners, including fibronectin, collagen, fibrillin-2, periostin, proteoglycans, and pathogens. Various transcription factors and intracellular regulators tightly regulate TNC expression. TNC plays an essential role in cell proliferation and migration. Unlike embryonic tissues, TNC protein is distributed over a few tissues in adults. However, higher TNC expression is observed in inflammation, wound healing, cancer, and other pathological conditions. It is widely expressed in a variety of human malignancies and is recognized as a pivotal factor in cancer progression and metastasis. Moreover, TNC increases both pro-and anti-inflammatory signaling pathways. It has been identified as an essential factor in tissue injuries such as damaged skeletal muscle, heart disease, and kidney fibrosis. This multimodular hexameric glycoprotein modulates both innate and adaptive immune responses regulating the expression of numerous cytokines. Moreover, TNC is an important regulatory molecule that affects the onset and progression of neuronal disorders through many signaling pathways. We provide a comprehensive overview of the structural and expression properties of TNC and its potential functions in physiological and pathological conditions.]]></description> </item><item><title><![CDATA[Evaluation of the Protective Effects of Vitamins E and D on Oxidative
Stress and Inflammation Caused by Tamoxifen in the Renal Tissue of
Female Wistar Rats]]></title><link>https://www.benthamscience.comarticle/134629</link><description><![CDATA[<p>Background: Tamoxifen is an effective drug for breast cancer treatment and its side effects are the production of reactive oxygen species and kidney damage. As antioxidants, vitamins E and D may help decrease kidney dysfunction. <p> Objectives: In the present study, the protective effects of vitamins E and D on renal toxicity caused by tamoxifen in female Wistar rats were investigated. <p> Materials and Methods: Twenty-five adult female rats weighing 180-200 were randomly divided into five groups with 5 rats. Group C, T, TE, TD, and TED were treated with olive oil, tamoxifen, tamoxifen + vitamin E, tamoxifen +vitamin D, and tamoxifen + both vitamins for four weeks. ELISA Kits measured the oxidant and antioxidant tests and TNF-&#945; in kidney tissue. The spectrophotometric method measured urea, uric acid, and creatinine in serum and urine. <p> Results: Tamoxifen significantly decreased the weight of rats, GPx, CAT, SOD levels and increased TNF-&#945;, urinary creatinine level and, serum uric acid, urea levels (P &#60; 0.05). But, treatment with vitamin D and simultaneous administration of vitamins led to a significant decrease in the level of (TNF-&#945;) compared to the tamoxifen group (p < 0.01). Also, the histopathology results showed that the simultaneous administration of vitamins has significantly resolved the damage caused by the use of tamoxifen. <p> Conclusion: The present study's findings showed that using vitamins E and D prevents kidney damage through antioxidant and anti-inflammatory effects. In addition, using vitamins E and D probably showed stronger synergistic effects against kidney damage.</p>]]></description> </item><item><title><![CDATA[Lysosomal Storage Diseases: Natural Products Inducing Autophagy]]></title><link>https://www.benthamscience.comarticle/134578</link><description><![CDATA[<p>Background: The link between autophagy and lysosomal function has been wellrecognised in recent decades; defective autophagy and lysosomal function lead to various disorders, notably Lysosomal Storage Disorders (LSDs). The malfunction of multiple mechanistic pathways influences the contribution of LSDs. Different ways are employed in such situations, but one novel approach could resolve the problem by inducing the autophagic pathway, which aids in maintaining proper autophagy and lysosomal degradation function. <p> Methods: Autophagic Inducer functions on the activation of Transcriptional factor EB (TFEB) and its mechanism; mTOR Complex Inhibition dependently or independently may repair the malfunction of the entire mechanism. Finding a potential autophagic inducer is still a work in progress, but targeting TFEB and mTOR could redefine LSD treatment. The development of experimentally available TFEB modulators could enhance autophagic flux promote lysosomal function and increase lysosomal biogenesis and can be a promising technique for treating illnesses caused by ALP dysfunction, such as lysosomal storage disorder. <p> Results: MTORC1 suppression causes TFEB to be transported to the nucleus and transcription of multiple genes involved in the formation of autophagosomes and lysosomes, indicating that MTORC1 has positive effects in treating lysosomal storage diseases such as Pompe disease, Batton disease, Fabry disease, etc. thus modulating autophagy attenuates the above condition. <p> Conclusion: This review comprises autophagy and lysosome association, and their malfunction leads to various lysosomal diseases. Several natural products are also discussed, which can be possible treatment options.</p>]]></description> </item><item><title><![CDATA[A Sustainable Approach Towards Prevention and Treatment of Hepatic
and Other Disorders Associated with Alcohol Consumption]]></title><link>https://www.benthamscience.comarticle/134585</link><description><![CDATA[<p>Background: Alcohol has been used for centuries in many different civilizations. It is a psychoactive stimulant with addictive properties. Alcohol misuse has significant negative social, economic, and health effects. Abusing alcohol can cause harm to oneself as well as to relatives, coworkers, close companions, and total strangers. Alcohol usage contributes to more than 200 diseases, accidents, and other health problems. Drinking alcohol is associated with a higher chance of developing significant non-communicable illnesses such liver cirrhosis, a number of cancers, cardiovascular diseases, as well as behavioral and mental disorders like alcoholism. <p> Objective: Abuse of alcohol does not occur suddenly. People becoming addicted to various alcoholic beverages is a problem that results from months and years of irresponsible drinking. The process of recovering from the issue in turn includes targeted, particular methods for raising awareness of the negative effects of alcohol usage. <p> Conclusion: Due to the heightened risks for one's bodily and mental health along with the social issues it generates, alcohol consumption results in these costs. We discuss the three areas of the epidemiology of alcohol's impact on health and diseases, the public health approach for treating problems related to alcohol use, and advancements in alcohol science.</p>]]></description> </item><item><title><![CDATA[miR-26a is a Key Therapeutic Target with Enormous Potential in the
Diagnosis and Prognosis of Human Disease]]></title><link>https://www.benthamscience.comarticle/137117</link><description><![CDATA[MicroRNA-26a (miR-26a) belongs to small non-coding regulatory RNA molecules emerging as fundamental post-transcriptional regulators inhibiting gene expression that plays vital roles in various processes of human diseases such as depression, renal ischemia and reperfusion injury, liver injury and some refractory cancer. In this review, we expound on the results of studies about miR-26a with emphasis on its function in animal models or <i>in vitro</i> cell culture to simulate the most common human disease in the clinic. Furthermore, we also illustrate the underlying mechanisms of miR-26a in strengthening the antitumor activity of antineoplastic drugs. Importantly, dysregulation of miR-26a has been related to many chronic and malignant diseases, especially in neurological disorders in the brain such as depression and neurodegenerative diseases as well as cancers such as papillary thyroid carcinoma, hepatocellular carcinoma and so on. It follows that miR-26a has a strong possibility to be a potential therapeutic target for the treatment of neurological disorders and cancers. Although the research of miRNAs has made great progress in the last few decades, much is yet to be discovered, especially regarding their underlying mechanisms and roles in the complex diseases of humans. Consequently, miR-26a has been analyzed in chronic and malignant diseases, and we discuss the dysregulation of miR-26a and functional roles in the development and pathogenesis of these diseases, which is very helpful for understanding their mechanisms as new biomarkers for diagnosing and curing diseases in the near future.]]></description> </item><item><title><![CDATA[Machine-learning-guided Directed Evolution for AAV Capsid Engineering]]></title><link>https://www.benthamscience.comarticle/138947</link><description><![CDATA[Target gene delivery is crucial to gene therapy. Adeno-associated virus (AAV) has emerged as a primary gene therapy vector due to its broad host range, long-term expression, and low pathogenicity. However, AAV vectors have some limitations, such as immunogenicity and insufficient targeting. Designing or modifying capsids is a potential method of improving the efficacy of gene delivery, but hindered by weak biological basis of AAV, complexity of the capsids, and limitations of current screening methods. Artificial intelligence (AI), especially machine learning (ML), has great potential to accelerate and improve the optimization of capsid properties as well as decrease their development time and manufacturing costs. This review introduces the traditional methods of designing AAV capsids and the general steps of building a sequence-function ML model, highlights the applications of ML in the development workflow, and summarizes its advantages and challenges.]]></description> </item><item><title><![CDATA[The Potential of Natural Products in the Management of Cardiovascular Disease]]></title><link>https://www.benthamscience.comarticle/138633</link><description><![CDATA[Cardiovascular Disease (CVD) is one of the most prevalent diseases in the world, comprising a variety of disorders such as hypertension, heart attacks, Peripheral Vascular Disease (PVD), dyslipidemias, strokes, coronary heart disease, and cardiomyopathies. The World Health Organization (WHO) predicts that 22.2 million people will die from CVD in 2030. Conventional treatments for CVDs are often quite expensive and also have several side effects. This potentiates the use of medicinal plants, which are still a viable alternative therapy for a number of diseases, including CVD. Natural products' cardio-protective effects result from their anti-oxidative, anti-hypercholesterolemia, anti-ischemic, and platelet aggregation-inhibiting properties. The conventional therapies used to treat CVD have the potential to be explored in light of the recent increase in the popularity of natural goods and alternative medicine. Some natural products with potential in the management of cardiovascular diseases such as <i>Allium sativum L., Ginkgo biloba, Cinchona ledgeriana, Ginseng, Commiphora mukul, Digitalis lanata, Digitalis purpurea L., Murrayakoenigii, Glycyrrhiza glabra, Polygonum cuspidatum, Fenugreek, Capsicum annuum</i>, etc. are discussed in this article.]]></description> </item><item><title><![CDATA[Pharmacological Considerations during Percutaneous Treatment of Heart
Failure]]></title><link>https://www.benthamscience.comarticle/138634</link><description><![CDATA[Heart Failure (HF) remains a global health challenge, marked by its widespread prevalence and substantial resource utilization. Although the prognosis has improved in recent decades due to the treatments implemented, it continues to generate high morbidity and mortality in the medium to long term. Interventional cardiology has emerged as a crucial player in HF management, offering a diverse array of percutaneous treatments for both acute and chronic HF. This article aimed to provide a comprehensive review of the role of percutaneous interventions in HF patients, with a primary focus on key features, clinical effectiveness, and safety outcomes. Despite the growing utilization of these interventions, there remain critical gaps in the existing body of evidence. Consequently, the need for high-quality randomized clinical trials and extensive international registries is emphasized to shed light on the specific patient populations and clinical scenarios that stand to benefit most from these innovative devices.]]></description> </item><item><title><![CDATA[A Comprehensive Review on Chemistry and Biology of Tafamidis in
Transthyretin Amyloidosis]]></title><link>https://www.benthamscience.comarticle/135146</link><description><![CDATA[Transthyretin amyloid cardiomyopathy and Transthyretin amyloid peripheral neuropathy are progressive disease conditions caused by Transthyretin amyloidosis (ATTR) fibril infiltration in the tissue. Transthyretin (TTR) protein misfolding and amyloid fibril deposits are pathological biomarkers of ATTR-related disorders. There are various treatment strategies targeting different stages in pathophysiology. One such strategy is TTR tetramer stabilization. Recently, a new TTR tetramer stabilizer, tafamidis, has been introduced that reduces the protein misfolding and amyloidosis and, consequently, disease progression in ATTR cardiomyopathy and peripheral neuropathy. This review will provide a comprehensive overview of the literature on tafamidis discovery, development, synthetic methods, pharmacokinetics, analytical methods and clinical trials. Overall, 7 synthetic methods, 5 analytical methods and 23 clinical trials have been summarized from the literature.]]></description> </item><item><title><![CDATA[Body Fat Distribution Contributes to Defining the Relationship between
Insulin Resistance and Obesity in Human Diseases]]></title><link>https://www.benthamscience.comarticle/133680</link><description><![CDATA[The risk for metabolic and cardiovascular complications of obesity is defined by body fat distribution rather than global adiposity. Unlike subcutaneous fat, visceral fat (including hepatic steatosis) reflects insulin resistance and predicts type 2 diabetes and cardiovascular disease. In humans, available evidence indicates that the ability to store triglycerides in the subcutaneous adipose tissue reflects enhanced insulin sensitivity. Prospective studies document an association between larger subcutaneous fat mass at baseline and reduced incidence of impaired glucose tolerance. Case-control studies reveal an association between genetic predisposition to insulin resistance and a lower amount of subcutaneous adipose tissue. Human peroxisome proliferator-activated receptorgamma (PPAR-γ) promotes subcutaneous adipocyte differentiation and subcutaneous fat deposition, improving insulin resistance and reducing visceral fat. Thiazolidinediones reproduce the effects of PPAR-γ activation and therefore increase the amount of subcutaneous fat while enhancing insulin sensitivity and reducing visceral fat. Partial or virtually complete lack of adipose tissue (lipodystrophy) is associated with insulin resistance and its clinical manifestations, including essential hypertension, hypertriglyceridemia, reduced HDL-c, type 2 diabetes, cardiovascular disease, and kidney disease. Patients with Prader Willi syndrome manifest severe subcutaneous obesity without insulin resistance. The impaired ability to accumulate fat in the subcutaneous adipose tissue may be due to deficient triglyceride synthesis, inadequate formation of lipid droplets, or defective adipocyte differentiation. Lean and obese humans develop insulin resistance when the capacity to store fat in the subcutaneous adipose tissue is exhausted and deposition of triglycerides is no longer attainable at that location. Existing adipocytes become large and reflect the presence of insulin resistance.]]></description> </item><item><title><![CDATA[An Overview of Diabetic Cardiomyopathy]]></title><link>https://www.benthamscience.comarticle/135183</link><description><![CDATA[Diabetic cardiomyopathy (DCM) is a myocardial disorder that is characterised by structural and functional abnormalities of the heart muscle in the absence of hypertension, valvular heart disease, congenital heart defects, or coronary artery disease (CAD). After witnessing a particular form of cardiomyopathy in diabetic individuals, Rubler <i>et al</i>. came up with the moniker diabetic cardiomyopathy in 1972. Four stages of DCM are documented, and the American College of Cardiology/American Heart Association Stage and New York Heart Association Class for HF have some overlap. Diabetes is linked to several distinct forms of heart failure. Around 40% of people with heart failure with preserved ejection fraction (HFpEF) have diabetes, which is thought to be closely associated with the pathophysiology of HFpEF. Diabetes and HF are uniquely associated in a bidirectional manner. When compared to the general population without diabetes, those with diabetes have a risk of heart failure that is up to four times higher. A biomarker is a trait that is reliably measured and assessed as a predictor of healthy biological activities, pathological processes, or pharmacologic responses to a clinical treatment. Several biomarker values have been discovered to be greater in patients with diabetes than in control subjects among those who have recently developed heart failure. Myocardial fibrosis and hypertrophy are the primary characteristics of DCM, and structural alterations in the diabetic myocardium are often examined by non-invasive, reliable, and reproducible procedures. An invasive method called endomyocardial biopsy (EMB) is most often used to diagnose many cardiac illnesses.]]></description> </item><item><title><![CDATA[Role of GLP-1 Receptor Agonist in Diabetic Cardio-renal Disorder:
Recent Updates of Clinical and Pre-clinical Evidence]]></title><link>https://www.benthamscience.comarticle/133503</link><description><![CDATA[Cardiovascular complications and renal disease is the growing cause of mortality in patients with diabetes. The subversive complications of diabetes such as hyperglycemia, hyperlipidemia and insulin resistance lead to an increase in the risk of myocardial infarction (MI), stroke, heart failure (HF) as well as chronic kidney disease (CKD). Among the commercially available anti-hyperglycemic agents, incretin-based medications appear to be safe and effective in the treatment of type 2 diabetes mellitus (T2DM) and associated cardiovascular and renal disease. Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have been shown to be fruitful in reducing HbA1c, blood glucose, lipid profile, and body weight in diabetic patients. Several preclinical and clinical studies revealed the safety, efficacy, and preventive advantages of GLP-1RAs against diabetes- induced cardiovascular and kidney disease. Data from cardio-renal outcome trials had highlighted that GLP-1RAs protected people with established CKD from significant cardiovascular disease, lowered the likelihood of hospitalization for heart failure (HHF), and lowered all-cause mortality. They also had a positive effect on people with end-stage renal disease (ESRD) and CKD. Beside clinical outcomes, GLP-1RAs reduced oxidative stress, inflammation, fibrosis, and improved lipid profile pre-clinically in diabetic models of cardiomyopathy and nephropathy that demonstrated the cardio-protective and reno-protective effect of GLP-1RAs. In this review, we have focused on the recent clinical and preclinical outcomes of GLP-1RAs as cardio-protective and reno-protective agents as GLP-1RAs medications have been demonstrated to be more effective in treating T2DM and diabetes-induced cardiovascular and renal disease than currently available treatments in clinics, without inducing hypoglycemia or weight gain.]]></description> </item><item><title><![CDATA[The Role of TRIM Proteins in Vascular Disease]]></title><link>https://www.benthamscience.comarticle/136249</link><description><![CDATA[There are more than 80 different tripartite motifs (TRIM) proteins within the E3 ubiquitin ligase subfamily, including proteins that regulate intracellular signaling, apoptosis, autophagy, proliferation, inflammation, and immunity through the ubiquitination of target proteins. Studies conducted in recent years have unraveled the importance of TRIM proteins in the pathophysiology of vascular diseases. In this review, we describe the effects of TRIM proteins on vascular endothelial cells, smooth muscle cells, heart, and lungs. In particular, we discuss the potential mechanisms by which TRIMs regulate diseases and shed light on the potential therapeutic applications of TRIMs.]]></description> </item><item><title><![CDATA[Role of LncRNA MIAT in Diabetic Complications]]></title><link>https://www.benthamscience.comarticle/134512</link><description><![CDATA[Long non-coding RNA (LncRNA) refers to a large class of RNAs with over 200 nucleotides that do not have the function of encoding proteins. In recent years, more and more literature has revealed that lncRNA is involved in manipulating genes related to human health and disease, playing outstanding biological functions, which has attracted widespread attention from researchers. The newly discovered long-stranded non-coding RNA myocardial infarction-related transcript (LncRNA MIAT) is abnormally expressed in a variety of diseases, especially in diabetic complications, and has been proven to have a wide range of effects. This review article aimed to summarize the importance of LncRNA MIAT in diabetic complications, such as diabetic cardiomyopathy, diabetic nephropathy, and diabetic retinopathy, and highlight the latest findings on the pathway and mechanism of its participation in regulating diabetic complications, which may aid in finding new intervention targets for the treatment of diabetic complications. LncRNA MIAT competitively binds microRNAs to regulate gene expression as competitive endogenous RNAs. Thus, this review article has reviewed the biological function and pathogenesis of LncRNA MIAT in diabetic complications and described its role in diabetic complications. This paper will help in finding new therapeutic targets and intervention strategies for diabetes complications.]]></description> </item><item><title><![CDATA[Free Radicals, Mitochondrial Dysfunction and Sepsis-induced Organ
Dysfunction: A Mechanistic Insight]]></title><link>https://www.benthamscience.comarticle/137503</link><description><![CDATA[Sepsis is a complex clinical condition and a leading cause of death worldwide. During Sepsis, there is a derailment in the host response to infection, which can progress to severe sepsis and multiple organ dysfunction or failure, which leads to death. Free radicals, including reactive oxygen species (ROS) generated predominantly in mitochondria, are one of the key players in impairing normal organ function in sepsis. ROS contributing to oxidative stress has been reported to be the main culprit in the injury of the lung, heart, liver, kidney, gastrointestinal, and other organs. Here in the present review, we describe the generation, and essential properties of various types of ROS, their effect on macromolecules, and their role in mitochondrial dysfunction. Furthermore, the mechanism involved in the ROS-mediated pathogenesis of sepsis-induced organ dysfunction has also been discussed.]]></description> </item><item><title><![CDATA[Acroparesthesias: An Overview]]></title><link>https://www.benthamscience.comarticle/135054</link><description><![CDATA[<p>Acroparesthesia is a symptom characterized by a subjective sensation, such as numbness, tingling, prickling, and reduced sensation, affecting the extremities (fingers and toes). Despite its frequency, data regarding its diagnostic approach and management are scarce. The etiological diagnosis of acroparesthesia is sometimes challenging since it can be due to abnormality anywhere along the sensory pathway from the peripheral nervous system to the cerebral cortex. Acroparesthesia can reveal several diseases. It can be associated with rheumatic complaints such as arthritis or myalgia. <p> Further cautions are required when paresthesia is acute (within days) in onset, rapidly progressive, severe, asymmetric, proximal, multifocal, or associated with predominant motor signs (limb weakness) or severe dysautonomia. Acroparesthesia may reveal Guillain-Barré syndrome or vasculitis, requiring rapid management. <p> Acroparesthesia is a predominant symptom of polyneuropathy, typically distal and symmetric, often due to diabetes. However, it can occur in other diseases such as vitamin B12 deficiency, monoclonal gammopathy of undetermined significance, or Fabry’s disease. Mononeuropathy, mainly carpal tunnel syndrome, remains the most common cause of acroparesthesia. <p> Ultrasonography contributes to the diagnosis of nerve entrapment neuropathy by showing nerve enlargement, hypoechogenic nerve, and intraneural vascularity. Besides, it can reveal its cause, such as space-occupying lesions, anatomical nerve variations, or anomalous muscle. Ultrasonography is also helpful for entrapment neuropathy treatment, such as ultrasound-guided steroid injection or carpal tunnel release. <p> The management of acroparesthesia depends on its causes. <p> This article aimed to review and summarize current knowledge on acroparesthesia and its causes. <p> We also propose an algorithm for the management of acroparesthesia.</p>]]></description> </item><item><title><![CDATA[Pathogenesis of the Left Ventricular Diastolic Dysfunction: The Immune
System Keeps Playing at the Backstage]]></title><link>https://www.benthamscience.comarticle/134422</link><description><![CDATA[]]></description> </item><item><title><![CDATA[NLRP3 Inflammasome: Key Role in the Pathophysiology of Cardiac Disorders
and its Potential as a Therapeutic Target]]></title><link>https://www.benthamscience.comarticle/135972</link><description><![CDATA[The NLRP3 inflammasome holds a pivotal position in the pathophysiological landscape of cardiac disorders, presenting itself as a promising therapeutic target. Central to this role are the proinflammatory cytokines Interleukin (IL)-1 and IL-18, which emerge as major players orchestrated by the activation of the NLRP3 inflammasome. This activation culminates in pyroptosis, a programmed form of cell death. While controlled activation of NLRP3 supports tissue repair, its excessive activation yields adverse consequences. Within the spectrum of cardiovascular diseases, ranging from abdominal aortic aneurysm to calcific aortic valve disease, the NLRP3 inflammasome is notably implicated. Atherosclerosis, myocardial infarction, diabetic cardiomyopathy, heart failure, and dilated cardiomyopathy collectively contribute to the genesis of inflammatory conditions. Key to this process is the nucleotide oligomerization domain-containing leucine-rich repeat protein 3 (NLRP3) inflammation, necessitating both priming and activation signals to orchestrate inflammation. Extensive scientific evidence substantiates the critical role of the NLRP3 inflammasome in cardiac disorders. Experimental models and clinical studies converge, highlighting its contribution to the intricate web of inflammatory pathways that underlie cardiac pathologies. This deeper understanding has spurred interest in targeting the NLRP3 inflammasome as a therapeutic avenue. Efforts to modulate the NLRP3 inflammasome are underway, aiming to temper its hyperactivity without disrupting its beneficial functions. Strategies involve small molecule inhibitors and biological agents, targeting various points along the signaling cascade. By selectively intervening in the NLRP3 pathway, researchers aspire to mitigate inflammatory responses, potentially ameliorating the progression of cardiac disorders. In conclusion, the NLRP3 inflammasome is a central orchestrator in the pathophysiology of diverse cardiac disorders. Its dual nature, capable of both driving repair and provoking harm, accentuates its significance as a therapeutic target. Scientific endeavors are actively unraveling its complexities, fostering the development of innovative interventions that could potentially revolutionize the management of cardiac inflammatory conditions.]]></description> </item><item><title><![CDATA[Mitochondrial Dysfunction in Neurodevelopmental Disorders: A Systematic
Review on Pathways and Mechanisms]]></title><link>https://www.benthamscience.comarticle/127433</link><description><![CDATA[<p>Background: Neurodevelopmental disorders (NDDs) are types of disorders that are marked by a wide range of genetic and clinical mutability which will affect the development and function of the brain. Mitochondria are increasingly associated with various neurodevelopmental disorders and it is found because of mutation of mitochondrial genes, which leads to mitochondrial dysfunction. <p> Objective: Understanding the pathways and mechanisms of mitochondrial dysfunction related to neurodevelopmental disorders such as ADHD, Pelizaeus- Merzbacher Disease (PMD), mental retardation, Autism spectrum disorder, Rett's syndrome, and Fragile X syndrome is important. In this review, we discussed the possible factors associated with mitochondria that influence the clinical presentation of NDDs, better understanding of the mechanisms behind these pathways will hopefully be helpful for the diagnosis and treatment approaches. <p> Conclusion: Mitochondria are simply another subcellular victim of various neurodegenerative pathways, or are they a common denominator on the path to neurodegeneration? A better understanding of functional and molecular mechanistic pathways can lead to the identification of potential targets, thereby opening perspectives for future treatment.</p>]]></description> </item><item><title><![CDATA[Marein Ameliorates Myocardial Fibrosis by Inhibiting HIF-1&#945; and
TGF-&#946;1/Smad2/3 Signaling Pathway in Isoproterenol-stimulated Mice and
TGF-&#946;1-stimulated Cardiac Fibroblasts]]></title><link>https://www.benthamscience.comarticle/136813</link><description><![CDATA[<p>Background: Myocardial fibrosis significantly contributes to the pathogenesis and progression of heart failure. <p> Objective: We probe into the impact of marein, a key bioactive compound in functional food Coreopsis tinctoria, on isoproterenol-stimulated myocardial fibrotic mice and transforming growth factor &#946;1 (TGF-&#946;1)-stimulated cardiac fibroblasts (CFs). <p> Methods: Isoproterenol was administered to the experimental mice via subcutaneous injection, and simultaneous administration of marein (25-100 mg/kg) was performed via oral gavage. CFs were stimulated with TGF- &#946;1 to trigger differentiation and collagen synthesis, followed by treatment with marein at concentrations of 5-20 μM. <p> Results: Treatment with marein in mice and CFs resulted in a significant reduction in the protein expression levels of &#945;-smooth muscle actin, collagen type I, and collagen type III. Additionally, marein treatment decreased the protein expression levels of TGF-&#946;1, hypoxia-inducible factor-1&#945; (HIF-1&#945;), p-Smad2/3, and Smad2/3. Notably, molecular docking analysis revealed that marein directly targets HIF-1&#945;. <p> Conclusion: Marein might exert a protective function in isoproterenol-stimulated myocardial fibrotic mice and TGF-&#946;1-stimulated CFs, which might result from the reduction of TGF-&#946;1 induced HIF-1&#945; expression, then inhibiting p-Smad2/3 and Smad2/3 expressions.</p>]]></description> </item><item><title><![CDATA[Deaths Due to Cardiomyopathy of Unknown Etiology in Children and
Young Adults]]></title><link>https://www.benthamscience.comarticle/122699</link><description><![CDATA[<p>Background: Cardiomyopathies are a group of diseases of the heart that can lead to heart failure, cardiac arrhythmia, and sudden death. They typically manifest as an enlarged heart or a normal heart with microscopic anomalies (fibrosis, inflammation, etc.). The aim of the study is to investigate the prevalence of deaths due to cardiomyopathies of unknown etiology in young subjects in a forensic pathology setting. <p> Materials and Methods: Deaths due to cardiomyopathy in decedents less than 40 years old evaluated at the Cook County Medical Examiner’s Office in Chicago from January 2013 to June 2018 were studied. <p> Results: In total, 140 cases of cardiomyopathies were identified in the study period: among these, in 20 cases (14%), no underlying etiology could be found through medical history and autopsy investigation. The demographics and the macroscopic and microscopic findings of these cases are described, highlighting the importance of medical history review and adequate histological sampling of hearts in cases of sudden, unexpected death in children and young adults. <p> Conclusion: This study highlights the importance of medical history review and adequate histological sampling of hearts in cases of sudden, unexpected death in children and young adults to identify possible cardiomyopathies of unknown etiology.</p>]]></description> </item><item><title><![CDATA[Antitumoral Potential of Artepillin C, a Compound Derived from Brazilian Propolis,
against Breast Cancer Cell Lines]]></title><link>https://www.benthamscience.comarticle/136016</link><description><![CDATA[<p>Background: Breast cancer is the most commonly diagnosed cancer among women worldwide with limited treatment options. Artepillin C (3,5-diprenyl-4-hydroxycinnamic acid) is one of the main constituents of Brazilian propolis presenting different activities, including antitumoral effects against various types of cancer. <p> Objective: We evaluated the antitumoral potential and mechanisms of action of artepillin C against two distinct human breast cancer cell lines, MCF-7 and MDA-MB-231, to explore a new therapeutic candidate. <p> Methods: Cell viability was assessed by MTT assay and the long-term cytotoxicity was performed by clonogenic assay. The morphological changes were observed by light microscopy, analysis of cell death pathway by Annexin V FITC/propidium iodide (PI), lactate dehydrogenase (LDH) by colorimetry, DNA fragmentation by agarose gel and senescence by β-galactosidase. Detection of total reactive oxygen species (ROS) by fluorescence microscopy and determination of mitochondrial transmembrane potential by flow cytometry were also performed. <p> Results: Artepillin C presented a strong and dose-time-dependent cytotoxic effect on MCF-7 and MDA-MB-231 cell lines, with cytotoxicity more evident in MCF-7. In both cancer cell lines, the clonogenic potential was significantly reduced and the morphology of the cells was changed. The treatment also induced death by necrosis and late apoptosis in MCF-7 and MDA-MB-231 and induced cell senescence in MCF-7. Also, artepillin C increased total ROS in both cancer cells and decreased mitochondrial membrane potential in MDA-MB-231 cells. <p> Conclusion: Artepillin C presented antitumoral potential in two human breast cancer cell lines, MCF-7, and MDA-MB-231, suggesting a new promising option for the treatment and/or chemopreventive strategy for breast cancer.</p>]]></description> </item><item><title><![CDATA[An Insight into the Pathogenesis of Diabetic Cardiomyopathy Along with
the Novel Potential Therapeutic Approaches]]></title><link>https://www.benthamscience.comarticle/131377</link><description><![CDATA[<p>Background: The existence of aberrant myocardial activity and function in the exclusion of those other cardiovascular events, such as atherosclerosis, hypertension, and severe valve disease, is known as diabetic cardiomyopathy. Diabetes patients are much more prone to death from cardiovascular illnesses than from any other cause, and they also have a 2–5 fold higher likelihood of acquiring cardiac failure and other complications. <p> Objective: In this review, the pathophysiology of diabetic cardiomyopathy is discussed, with an emphasis on the molecular and cellular irregularities that arise as the condition progresses, as well as existing and prospective future treatments. <p> Method: The literature for this topic was researched utilizing Google Scholar as a search engine. Before compiling the review article, several research and review publications from various publishers, including Bentham Science, Nature, Frontiers, and Elsevier, were investigated. <p> Result: The abnormal cardiac remodelling, marked by left ventricular concentric thickening and interstitial fibrosis contributing to diastolic impairment, is mediated by hyperglycemia, and insulin sensitivity. The pathophysiology of diabetic cardiomyopathy has been linked to altered biochemical parameters, decreased calcium regulation and energy production, enhanced oxidative damage and inflammation, and a build-up of advanced glycation end products. <p> Conclusion: Antihyperglycemic medications are essential for managing diabetes because they successfully lower microvascular problems. GLP-1 receptor agonists and sodium-glucose cotransporter 2 inhibitors have now been proven to benefit heart health by having a direct impact on the cardiomyocyte. To cure and avoid diabetic cardiomyopathy new medicines are being researched, including miRNA and stem cell therapies.</p>]]></description> </item><item><title><![CDATA[New Insights into the Long Non-coding RNAs Dependent Modulation
of Heart Failure and Cardiac Hypertrophy: From Molecular
Function to Diagnosis and Treatment]]></title><link>https://www.benthamscience.comarticle/130023</link><description><![CDATA[Heart failure (HF) is a public health issue that imposes high costs on healthcare systems. Despite the significant advances in therapies and prevention of HF, it remains a leading cause of morbidity and mortality worldwide. The current clinical diagnostic or prognostic biomarkers, as well as therapeutic strategies, have some limitations. Genetic and epigenetic factors have been identified to be central to the pathogenesis of HF. Therefore, they might provide promising novel diagnostic and therapeutic approaches for HF. Long non-coding RNAs (lncRNAs) belong to a group of RNAs that are produced by RNA polymerase II. These molecules play an important role in the functioning of different cell biological processes, such as transcription and regulation of gene expression. LncRNAs can affect different signaling pathways by targeting biological molecules or a variety of different cellular mechanisms. The alteration in their expression has been reported in different types of cardiovascular diseases, including HF, supporting the theory that they are important in the development and progression of heart diseases. Therefore, these molecules can be introduced as diagnostic, prognostic, and therapeutic biomarkers in HF. In this review, we summarize different lncRNAs as diagnostic, prognostic, and therapeutic biomarkers in HF. Moreover, we highlight various molecular mechanisms dysregulated by different lncRNAs in HF.]]></description> </item><item><title><![CDATA[Chinese Medicine Supplementing Qi and Activating Blood Circulation
Relieves the Progression of Diabetic Cardiomyopathy]]></title><link>https://www.benthamscience.comarticle/131348</link><description><![CDATA[<p>Background: Diabetic cardiomyopathy (DCM) is the leading cause of diabetic death as the final occurrence of heart failure and arrhythmia. Traditional Chinese medicine is usually used to treat various diseases including diabetes. <p> Objective: This study sought to investigate the effects of Traditional Chinese medicine supplementing Qi and activating blood circulation (SAC) in DCM. <p> Methods: After the construction of the DCM model by streptozotocin (STZ) injection and high glucose/fat diet feeding, rats were administered intragastrically with SAC. Then, cardiac systolic/diastolic function was evaluated by detecting left ventricular systolic pressure (LVSP), maximal rate of left ventricular pressure rise (+LVdp/dtmax), and fall (-LVdp/dtmax), heart rate (HR), left ventricular ejection fraction (EF), LV fractional shortening (FS) and left ventricular end-diastolic pressure (LVEDP). Masson’s and TUNEL staining were used to assess fibrosis and cardiomyocyte apoptosis. <p> Results: DCM rats exhibited impaired cardiac systolic/diastolic function manifested by decreasing LVSP, + LVdp/dtmax, -LVdp/dtmax, HR, EF and FS, and increasing LVEDP. Intriguingly, traditional Chinese medicine SAC alleviated the above-mentioned symptoms, indicating a potential role in improving cardiac function. Masson’s staining substantiated that SAC antagonized the increased collagen deposition and interstitial fibrosis area and the elevations in protein expression of fibrosisrelated collagen I and fibronectin in heart tissues of DCM rats. Furthermore, TUNEL staining confirmed that traditional Chinese medicine SAC also attenuated cardiomyocyte apoptosis in DCM rats. Mechanically, DCM rats showed the aberrant activation of the TGF-&#946;/Smad signaling, which was inhibited after SAC. <p> Conclusion: SAC may exert cardiac protective efficacy in DCM rats via the TGF-&#946;/Smad signaling, indicating a new promising therapeutic approach for DCM.</p>]]></description> </item><item><title><![CDATA[Microbubbles: Revolutionizing Biomedical Applications with Tailored
Therapeutic Precision]]></title><link>https://www.benthamscience.comarticle/136811</link><description><![CDATA[<P>Background: Over the past ten years, tremendous progress has been made in microbubble-based research for a variety of biological applications. Microbubbles emerged as a compelling and dynamic tool in modern drug delivery systems. They are employed to deliver drugs or genes to targeted regions of interest, and then ultrasound is used to burst the microbubbles, causing site-specific delivery of the bioactive materials. <P> Objective: The objective of this article is to review the microbubble compositions and physiochemical characteristics in relation to the development of innovative biomedical applications, with a focus on molecular imaging and targeted drug/gene delivery. <P> Methods: The microbubbles are prepared by using various methods, which include cross-linking polymerization, emulsion solvent evaporation, atomization, and reconstitution. In cross-linking polymerization, a fine foam of the polymer is formed, which serves as a bubble coating agent and colloidal stabilizer, resulting from the vigorous stirring of a polymeric solution. In the case of emulsion solvent evaporation, there are two solutions utilized in the production of microbubbles. In atomization and reconstitution, porous spheres are created by atomising a surfactant solution into a hot gas. They are encapsulated in primary modifier gas. After the addition of the second gas or gas osmotic agent, the package is placed into a vial and sealed after reconstituting with sterile saline solution. <P> Results: Microbubble-based drug delivery is an innovative approach in the field of drug delivery that utilizes microbubbles, which are tiny gas-filled bubbles, act as carriers for therapeutic agents. These microbubbles can be loaded with drugs, imaging agents, or genes and then guided to specific target sites. <P> Conclusion: The potential utility of microbubbles in biomedical applications is continually growing as novel formulations and methods. The versatility of microbubbles allows for customization, tailoring the delivery system to various medical applications, including cancer therapy, cardiovascular treatments, and gene therapy.</P>]]></description> </item><item><title><![CDATA[CRISPR-Cas9 for the Treatment of Transthyretin Cardiac Amyloidosis]]></title><link>https://www.benthamscience.comarticle/136535</link><description><![CDATA[]]></description> </item><item><title><![CDATA[Role of Vitamins in Cardiovascular Health: Know Your Facts-Part 2]]></title><link>https://www.benthamscience.comarticle/134401</link><description><![CDATA[Cardiovascular disease (CVD) is a major cause of morbidity/mortality world-wide, hence preventive interventions are crucial. Observational data showing beneficial CV effects of vitamin supplements, promoted by self-proclaimed experts, have led to ~50% of Americans using multivitamins; this practice has culminated into a multi-billion-dollar business. However, robust evidence is lacking, and certain vitamins might incur harm. This two-part review focuses on the attributes or concerns about specific vitamin consumption on CVD. The evidence for indiscriminate use of multivitamins indicates no consistent CVD benefit. Specific vitamins and/or combinations are suggested, but further supportive evidence is needed. Data presented in Part 1 indicated that folic acid and certain B-vitamins may decrease stroke, whereas niacin might raise mortality; beta-carotene mediates pro-oxidant effects, which may abate the benefits from other vitamins. In Part 2, data favor the anti-oxidant effects of vitamin C and the anti-atherogenic effects of vitamins C and E, but clinical evidence is inconsistent. Vitamin D may provide CV protection, but data are conflicting. Vitamin K appears neutral. Thus, there are favorable CV effects of individual vitamins (C/D), but randomized/controlled data are lacking. An important caveat regards the potential toxicity of increased doses of fat-soluble vitamins (A/D/E/K). As emphasized in Part 1, vitamins might benefit subjects who are antioxidant-deficient or exposed to high levels of oxidative-stress (e.g., diabetics, smokers, and elderly), stressing the importance of targeting certain subgroups for optimal results. Finally, by promoting CV-healthy balanced-diets, we could acquire essential vitamins and nutrients and use supplements only for specific indications.]]></description> </item><item><title><![CDATA[Stem Cell-based Therapies in Cardiovascular Diseases: From Pathophysiology
to Clinical Outcomes]]></title><link>https://www.benthamscience.comarticle/134094</link><description><![CDATA[Over 20 years of intensified research in the field of stem cells brought about unprecedented possibilities in treating heart diseases. The investigators were initially fascinated by the idea of regenerating the lost myocardium and replacing it with new functional cardiomyocytes, but this was extremely challenging. However, the multifactorial effects of stem cell-based therapies beyond mere cardiomyocyte generation, caused by paracrine signaling, would open up new possibilities in treating cardiovascular diseases. To date, there is a strong body of evidence that the anti-inflammatory, anti-apoptotic, and immunomodulatory effects of stem cell therapy may alleviate atherosclerosis progression. In the present review, our objective is to provide a brief overview of the stem cell-based therapeutic options. We aim to delineate the pathophysiological mechanisms of their beneficial effects in cardiovascular diseases especially in coronary artery disease and to highlight some conclusions from important clinical studies in the field of regenerative medicine in cardiovascular diseases and how we could further move onwards.]]></description> </item><item><title><![CDATA[The (Pro)renin Receptor - A Regulatory Nodal Point in Disease Networks]]></title><link>https://www.benthamscience.comarticle/135585</link><description><![CDATA[<P>Experimental inhibition of the (pro)renin receptor [(P)RR] is a promising therapeutic strategy in different disease models ranging from cardiorenal to oncological entities. Here, we briefly review the direct protein-protein interaction partners of the (P)RR and the plethora of distinct diseases in which the (P)RR is involved. <P> The first structural work on the (P)RR using AlphaFold, which was recently published by Ebihara et al., is the center of this mini-review since it can mechanistically link the protein-protein interaction level with the pathophysiological level. <P> More detailed insights into the 3D structure of the (P)RR and its interaction domains might guide drug discovery on this novel target. Finally, antibody- and small molecule-based approaches to inhibit the (P)RR are shortly discussed.</P>]]></description> </item><item><title><![CDATA[RNA Interference and Neuromuscular Diseases: A Focus on Hereditary
Transthyretin Amyloidosis]]></title><link>https://www.benthamscience.comarticle/134496</link><description><![CDATA[Neuromuscular diseases are severe disorders affecting the peripheral nervous system, usually driving to death in a limited time. Many new drugs, through RNA-interference technology, are revolutionizing the prognosis and quality of life for these patients. Nevertheless, given the increased life expectancy, some new issues and phenotypes are expected to be revealed. In the transthyretin-mediated hereditary amyloidosis (ATTR-v, \"v\" for \"variant\"), the RNA interference was demonstrated to effectively reduce the hepatic synthesis of transthyretin, with a significant increase in disease progression in terms of polyneuropathy and cardiomyopathy. The increased life expectancy could promote the involvement of organs where the extra-hepatic transthyretin is deposited, such as the brain and eye, which are probably not targeted by the available treatments. All these issues are discussed in this editorial.]]></description> </item><item><title><![CDATA[Impact of Breaking up of Sitting Time on Anti-inflammatory Response
Induced by Extracellular Vesicles]]></title><link>https://www.benthamscience.comarticle/135637</link><description><![CDATA[Physical inactivity and sedentary behaviors (SB) have promoted a dramatic increase in the incidence of a host of chronic disorders over the last century. The breaking up of sitting time (<i>i.e.</i>, sitting to standing up transition) has been proposed as a promising solution in several epidemiological and clinical studies. In parallel to the large interest it initially created, there is a growing body of evidence indicating that breaking up prolonged sedentary time (<i>i.e</i>., > 7 h in sitting time) could reduce overall mortality risks by normalizing the inflammatory profile and cardiometabolic functions. Recent advances suggest that the latter health benefits, may be mediated through the immunomodulatory properties of extracellular vesicles. Primarily composed of miRNA, lipids, mRNA and proteins, these vesicles would influence metabolism and immune system functions by promoting M1 to M2 macrophage polarization (<i>i.e.</i>, from a pro-inflammatory to anti-inflammatory phenotype) and improving endothelial function. The outcomes of interrupting prolonged sitting time may be attributed to molecular mechanisms induced by circulating angiogenic cells. Functionally, circulating angiogenic cells contribute to repair and remodel the vasculature. This effect is proposed to be mediated through the secretion of paracrine factors. The present review article intends to clarify the beneficial contributions of breaking up sitting time on extracellular vesicles formation and macrophage polarization (M1 and M2 phenotypes). Hence, it will highlight key mechanistic information regarding how breaking up sitting time protocols improves endothelial health by promoting antioxidant and anti-inflammatory responses in human organs and tissues.]]></description> </item><item><title><![CDATA[Rosuvastatin Improves Endothelial Dysfunction in Diabetes by Normalizing
Endoplasmic Reticulum Stress <i>via</i> Calpain-1 Inhibition]]></title><link>https://www.benthamscience.comarticle/135433</link><description><![CDATA[<p>Background: Rosuvastatin contributes to the improvement of vascular complications in diabetes, but the protective mechanisms remain unclear. The aim of the present study was to investigate the effect and mechanism of rosuvastatin on endothelial dysfunction induced by diabetes. <p> Methods: Calpain-1 knockout (Capn1 EK684-/-) and C57BL/6 mice were intraperitoneally injected with STZ to induce type 1 diabetes. Human umbilical vein endothelial cells (HUVECs) were incubated with high glucose in this study. The function of isolated vascular rings, apoptosis, and endoplasmic reticulum stress (ERS) indicators were measured in this experiment. <p> Results: The results showed that rosuvastatin (5 mg/kg/d) and calpain-1 knockout improved impaired vasodilation in an endothelial-dependent manner, and this effect was abolished by an ERS inducer. Rosuvastatin administration inhibited calpain-1 activation and ERS induced by high glucose, as well as apoptosis and oxidative stress both in vivo and in vitro. In addition, an ERS inducer (tunicamycin) offset the beneficial effect of rosuvastatin on endothelial dysfunction and ERS, which was accompanied by increased calpain-1 expression. The ERS inhibitor showed a similar improvement in endothelial dysfunction with rosuvastatin but could not increase the improvement in endothelial function of rosuvastatin. <p> Conclusion: These results suggested that rosuvastatin improves endothelial dysfunction by suppressing calpain- 1 and normalizing ERS, subsequently decreasing apoptosis and oxidative stress.</p>]]></description> </item><item><title><![CDATA[Is Adrenaline Always the First Choice Therapy of Anaphylaxis? An
Allergist-cardiologist Interdisciplinary Point of View]]></title><link>https://www.benthamscience.comarticle/135548</link><description><![CDATA[Worldwide, adrenaline is considered the first choice therapy in the international guidelines for the management of anaphylaxis. However, the heart and cardiovascular apparatus are strongly involved in anaphylaxis; for that reason, there are some cardiac conditions and certain anaphylaxis patterns that make epinephrine use problematic without adequate heart monitoring. The onset of Kounis syndrome, takotsubo cardiopathy, or the paradoxical anaphylaxis require great attention in the management of anaphylaxis and adrenaline administration by clinicians, who should be aware of the undervalued evolution of anaphylaxis and the potential cardiologic complications of epinephrine administration. Numerous case reports and studies describe the unexpected onset of cardiac diseases following epinephrine treatment, despite the latter being the recommended therapy for anaphylaxis. Our review suggests that future anaphylaxis guidelines should incorporate cardiovascular specialists since the treatment of Kounis syndrome or takotsubo cardiopathy requires cardiologist skills.]]></description> </item></channel></rss>