Title:Mitochondrial Dysfunction in Cardiac Diseases: Insights into Pathophysiology and Clinical Outcomes
Volume: 22
Issue: 1
Author(s): Syed Shadab Ahmad, Javed Akhtar Ansari*, Tarique Mahmood Ansari and Syed Mehdi Hasan Zaidi
Affiliation:
- Faculty of Pharmacy, Integral University, Kursi Road, Lucknow, 226026, India
Keywords:
Mitochondrial dysfunction, cardiac toxicity, cardiomyopathy, cardiovascular diseases, fatty acids, adenosine triphosphate.
Abstract: Mitochondrial dysfunction plays a crucial role in the pathogenesis of various cardiac
diseases, including heart failure, ischemic cardiomyopathy, and drug-induced cardiotoxicity.
Mitochondria are essential for cellular energy production, calcium homeostasis, redox balance,
and apoptotic regulation, making their proper function vital for cardiac health. Dysfunctional
mitochondria contribute to excessive reactive oxygen species (ROS) production, impaired ATP
synthesis, and disruption of mitochondrial dynamics, leading to cardiomyocyte damage and cell
death. Emerging research highlights mitochondrial dynamics, including fission, fusion,
mitophagy, and biogenesis, as critical determinants of cardiac homeostasis. Perturbations in
these processes exacerbate myocardial injury and heart failure progression. Additionally,
chemotherapy-induced cardiotoxicity, primarily from anthracyclines, is closely linked to
mitochondrial damage, underscoring the need for targeted therapeutic strategies.
Pharmacological interventions, such as antioxidants, mitochondrial-targeted drugs, and
cardioprotective agents, have shown promise in mitigating mitochondrial dysfunction-related
cardiac toxicity. Furthermore, lifestyle modifications, including exercise and dietary
interventions, are being explored to enhance mitochondrial resilience in cardiac tissues.
Advanced imaging techniques and biomarker-based diagnostics are improving the early
detection of mitochondrial dysfunction in cardiac diseases. Emerging therapeutic strategies, such
as mitochondrial transplantation, gene therapy, and precision medicine approaches, hold
potential for targeted intervention. Despite these advances, challenges remain in translating
mitochondrial-targeted therapies into clinical practice due to complexities in mitochondrial regulation
and inter-organ communication. Future research should focus on optimizing mitochondrial-targeted
interventions, improving diagnostic precision, and exploring novel molecular pathways to mitigate
cardiac mitochondrial dysfunction. A comprehensive understanding of mitochondrial pathophysiology
in cardiac diseases will pave the way for innovative treatment strategies aimed at preserving cardiac
function and reducing the burden of heart failure.
