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Current Aging Science

Editor-in-Chief

ISSN (Print): 1874-6098
ISSN (Online): 1874-6128

Mini-Review Article

Mitochondrial Ion Channels in Aging and Related Diseases

Author(s): Md. Ashrafuzzaman*

Volume 15, Issue 2, 2022

Published on: 21 April, 2022

Page: [97 - 109] Pages: 13

DOI: 10.2174/1874609815666220119094324

Price: $65

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Abstract

Transport of materials and information across cellular boundaries, such as plasma, mitochondrial and nuclear membranes, happens mainly through varieties of ion channels and pumps. Various biophysical and biochemical processes play vital roles. The underlying mechanisms and associated phenomenological lipid membrane transports are linked directly or indirectly to the cell health condition. Mitochondrial membranes (mitochondrial outer membrane (MOM) and mitochondrial inner membrane (MIM)) host crucial cellular processes. Their malfunction is often found responsible for the rise of cell-originated diseases, including cancer, Alzheimer’s, neurodegenerative disease, etc. A large number of ion channels active across MOM and MIM are known to belong to vital cell-based structures found to be linked directly to cellular signaling. Hence, their malfunctions are often found to contribute to abnormalities in intracellular communication, which may even be associated with the rise of various diseases. This article aims to pinpoint ion channels that are directly or indirectly linked to especially aging and related abnormalities in health conditions. An attempt has been made to address the natural structures of these channels, their mutated conditions, and the ways we may cause interventions in their malfunctioning. The malfunction of ion channel subunits, especially various proteins, involved directly in channel formation and/or indirectly in channel stabilization leads to the rise of various channel-specific diseases, which are known as channelopathies. Channelopathies in aging will be discussed briefly. This mini-review may be found as an important reference for drug discovery scientists dealing with aging-related diseases.

Keywords: Ion channels, mitochondrial membrane, membrane potential, disease, aging, channelopathy.

Graphical Abstract
[1]
Purves D, Augustine GJ, Fitzpatrick D, Eds. , et al.Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates 2001.
[2]
Minor DL Jr. An overview of ion channel structure. In: Ralph AB, Edward AD, Eds.Handbook of Cell Signaling Cambridge, Massachu-setts. United States: Academic Press 2010; pp. 201-7.
[http://dx.doi.org/10.1016/B978-0-12-374145-5.00030-9]
[3]
Rose MR. Neurological channelopathies. BMJ 1998; 316(7138): 1104-5.
[http://dx.doi.org/10.1136/bmj.316.7138.1104] [PMID: 9552942]
[4]
Marín-García J, Goldenthal MJ, Moe GW. Cardiac dysrhythmias and channelopathies in aging. In: Marín-García J, Goldenthal MJ, Moe GW, Eds.Aging and the Heart. Boston, MA: Springer 2008.
[http://dx.doi.org/10.1007/978-0-387-74072-0_11]
[5]
Kim JB. Channelopathies. Korean J Pediatr 2014; 57(1): 1-18.
[http://dx.doi.org/10.3345/kjp.2014.57.1.1] [PMID: 24578711]
[6]
Ashrafuzzaman M. Biophysics and Nanotechnology of Ion Channels. 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL: CRC Press (Taylor and Francis Group) 2021.
[http://dx.doi.org/10.1201/9781003010654]
[7]
Ashrafuzzaman M, Lampson MA, Greathouse DV, Koeppe RE, Andersen OS. Manipulating lipid bilayer material properties using biologi-cally active amphipathic molecules. J Phys Condens Matter 2006; 18: S1235-55.
[http://dx.doi.org/10.1088/0953-8984/18/28/S08]
[8]
Bitler A, Dover R, Shai Y. Anticancer drug colchicine increases disorder and reduces complexity in the macrophage membrane. Biophys J 2016; 110: 83A.
[http://dx.doi.org/10.1016/j.bpj.2015.11.507]
[9]
Ashrafuzzaman M. Amphiphiles capsaicin and triton X-100 regulate the chemotherapy drug colchicine’s membrane adsorption and ion pore formation potency. Saudi J Biol Sci 2021; 28(5): 3100-9.
[http://dx.doi.org/10.1016/j.sjbs.2021.02.054] [PMID: 34025185]
[10]
Ashrafuzzaman M. The antimicrobial peptide gramicidin s enhances membrane adsorption and ion pore formation potency of chemother-apy drugs in lipid bilayers. Membranes (Basel) 2021; 11(4): 247.
[http://dx.doi.org/10.3390/membranes11040247] [PMID: 33808204]
[11]
Ackerman MJ, Clapham DE. Ion channels-basic science and clinical disease. N Engl J Med 1997; 336(22): 1575-86.
[http://dx.doi.org/10.1056/NEJM199705293362207] [PMID: 9164815]
[12]
Hanna MG, Wood NW, Kullmann DM. Ion channels and neurological disease: DNA based diagnosis is now possible, and ion channels may be important in common paroxysmal disorders. J Neurol Neurosurg Psychiatry 1998; 65(4): 427-31.
[http://dx.doi.org/10.1136/jnnp.65.4.427] [PMID: 9771758]
[13]
Spillane J, Kullmann DM, Hanna MG. Genetic neurological channelopathies: Molecular genetics and clinical phenotypes. J Neurol Neurosurg Psychiatry 2016; 7: 37-48.
[http://dx.doi.org/10.1136/jnnp-2015-311233] [PMID: 26558925]
[14]
O’Rourke B. Mitochondrial ion channels. Annu Rev Physiol 2007; 69: 19-49.
[http://dx.doi.org/10.1146/annurev.physiol.69.031905.163804] [PMID: 17059356]
[15]
Malli R, Graier WF. Mitochondrial Ca2+ channels: Great unknowns with important functions. FEBS Lett 2010; 584(10): 1942-7.
[http://dx.doi.org/10.1016/j.febslet.2010.01.010] [PMID: 20074570]
[16]
Urbani A, Prosdocimi E, Carrer A, Checchetto V, Szabò I. Mitochondrial ion channels of the inner membrane and their regulation in cell death signaling. Front Cell Dev Biol 2021; 8: 620081.
[http://dx.doi.org/10.3389/fcell.2020.620081] [PMID: 33585458]
[17]
Bock FJ, Tait SWG. Mitochondria as multifaceted regulators of cell death. Nat Rev Mol Cell Biol 2020; 21(2): 85-100.
[http://dx.doi.org/10.1038/s41580-019-0173-8] [PMID: 31636403]
[18]
Bortner CD, Cidlowski JA. Ion channels and apoptosis in cancer. Philos Trans R Soc Lond B Biol Sci 2014; 369(1638): 20130104.
[http://dx.doi.org/10.1098/rstb.2013.0104] [PMID: 24493752]
[19]
Kondratskyi A, Kondratska K, Skryma R, Prevarskaya N. Ion channels in the regulation of apoptosis. Biochim Biophys Acta 2015; 1848(10 Pt B): 2532-46.
[http://dx.doi.org/10.1016/j.bbamem.2014.10.030] [PMID: 25450339]
[20]
Leanza L, Managò A, Zoratti M, Gulbins E, Szabo I. Pharmacological targeting of ion channels for cancer therapy: In vivo evidences. Biochim Biophys Acta 2016; 1863(6 Pt B): 1385-97.
[http://dx.doi.org/10.1016/j.bbamcr.2015.11.032] [PMID: 26658642]
[21]
Fricker M, Tolkovsky AM, Borutaite V, Coleman M, Brown GC. Neuronal cell death. Physiol Rev 2018; 98(2): 813-80.
[http://dx.doi.org/10.1152/physrev.00011.2017] [PMID: 29488822]
[22]
Bachmann M, Pontarin G, Szabo I. The contribution of mitochondrial ion channels to cancer development and progression. Cell Physiol Biochem 2019; 53(S1): 63-78.
[http://dx.doi.org/10.33594/000000198] [PMID: 31860207]
[23]
Felix R. Channelopathies: Ion channel defects linked to heritable clinical disorders. J Med Genet 2000; 37(10): 729-40.
[http://dx.doi.org/10.1136/jmg.37.10.729] [PMID: 11015449]
[24]
Enkvetchakul D. Genetic disorders of ion channels. Mo Med 2010; 107(4): 270-5.
[PMID: 20806840]
[25]
Steinlein OK. Ion channel mutations in neuronal diseases: a genetics perspective. Chem Rev 2012; 112(12): 6334-52.
[http://dx.doi.org/10.1021/cr300044d] [PMID: 22607259]
[26]
Pi Y, Goldenthal MJ, Marín-García J. Mitochondrial channelopathies in aging. J Mol Med (Berl) 2007; 85(9): 937-51.
[http://dx.doi.org/10.1007/s00109-007-0190-5] [PMID: 17426949]
[27]
Brown MR, Geddes JW, Sullivan PG. Brain region-specific, age-related, alterations in mitochondrial responses to elevated calcium. J Bioenerg Biomembr 2004; 36(4): 401-6.
[http://dx.doi.org/10.1023/B:JOBB.0000041775.10388.23] [PMID: 15377879]
[28]
Panel M, Ghaleh B, Morin D. Mitochondria and aging: A role for the mitochondrial transition pore? Aging Cell 2018; 17(4): e12793.
[http://dx.doi.org/10.1111/acel.12793] [PMID: 29888494]
[29]
Muqit MM, Gandhi S, Wood NW. Mitochondria in Parkinson disease: Back in fashion with a little help from genetics. Arch Neurol 2006; 63(5): 649-54.
[http://dx.doi.org/10.1001/archneur.63.5.649] [PMID: 16682534]
[30]
Winklhofer KF, Haass C. Mitochondrial dysfunction in Parkinson’s disease. Biochim Biophys Acta 2010; 1802(1): 29-44.
[http://dx.doi.org/10.1016/j.bbadis.2009.08.013] [PMID: 19733240]
[31]
Exner N, Lutz AK, Haass C, Winklhofer KF. Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysio-logical consequences. EMBO J 2012; 31(14): 3038-62.
[http://dx.doi.org/10.1038/emboj.2012.170] [PMID: 22735187]
[32]
Chen C, Turnbull DM, Reeve AK. Mitochondrial dysfunction in parkinson’s disease-cause or consequence? Biology (Basel) 2019; 8(2): 38.
[http://dx.doi.org/10.3390/biology8020038] [PMID: 31083583]
[33]
Nicoletti V, Palermo G, Del Prete E, Mancuso M, Ceravolo R. Understanding the multiple role of mitochondria in parkinson’s disease and related disorders: lesson from genetics and protein-interaction network. Front Cell Dev Biol 2021; 9: 636506.
[http://dx.doi.org/10.3389/fcell.2021.636506] [PMID: 33869180]
[34]
Peixoto PM, Ryu SY, Kinnally KW. Mitochondrial ion channels as therapeutic targets. FEBS Lett 2010; 584(10): 2142-52.
[http://dx.doi.org/10.1016/j.febslet.2010.02.046] [PMID: 20178788]
[35]
Parrasia S, Mattarei A, Furlan A, Zoratti M, Biasutto L. Small-molecule modulators of mitochondrial channels as chemotherapeutic agents. Cell Physiol Biochem 2019; 53(S1): 11-43.
[http://dx.doi.org/10.33594/000000192] [PMID: 31834993]
[36]
Hausenloy DJ, Schulz R, Girao H, et al. Mitochondrial ion channels as targets for cardioprotection. J Cell Mol Med 2020; 24(13): 7102-14.
[http://dx.doi.org/10.1111/jcmm.15341] [PMID: 32490600]
[37]
Szabo I, Zoratti M, Biasutto L. Targeting mitochondrial ion channels for cancer therapy. Redox Biol 2021; 42: 101846.
[http://dx.doi.org/10.1016/j.redox.2020.101846] [PMID: 33419703]
[38]
Simms BA, Zamponi GW. Neuronal voltage-gated calcium channels: structure, function, and dysfunction. Neuron 2014; 82(1): 24-45.
[http://dx.doi.org/10.1016/j.neuron.2014.03.016] [PMID: 24698266]
[39]
Kumar P, Kumar D, Jha SK, Jha NK, Ambasta RK. Ion channels in neurological disorders. Adv Protein Chem Struct Biol 2016; 103: 97-136.
[http://dx.doi.org/10.1016/bs.apcsb.2015.10.006] [PMID: 26920688]
[40]
Rice RA, Berchtold NC, Cotman CW, Green KN. Age-related downregulation of the CaV3.1 T-type calcium channel as a mediator of amy-loid beta production. Neurobiol Aging 2014; 35(5): 1002-11.
[http://dx.doi.org/10.1016/j.neurobiolaging.2013.10.090] [PMID: 24268883]
[41]
Lin AH, Liu MH, Ko HK, Perng DW, Lee TS, Kou YR. Lung epithelial trpa1 transduces the extracellular ros into transcriptional regulation of lung inflammation induced by cigarette smoke: The role of influxed Ca². Mediators Inflamm 2015; 2015: 148367.
[http://dx.doi.org/10.1155/2015/148367] [PMID: 26504357]
[42]
Schilling T, Eder C. Microglial K(+) channel expression in young adult and aged mice. Glia 2015; 63(4): 664-72.
[http://dx.doi.org/10.1002/glia.22776] [PMID: 25472417]
[43]
Lam A, Karekar P, Shah K, et al. Drosophila voltage-gated calcium channel α1-subunits regulate cardiac function in the aging heart. Sci Rep 2018; 8(1): 6910.
[http://dx.doi.org/10.1038/s41598-018-25195-0] [PMID: 29720608]
[44]
Jones JL, Peana D, Veteto AB, et al. TRPV4 increases cardiomyocyte calcium cycling and contractility yet contributes to damage in the aged heart following hypoosmotic stress. Cardiovasc Res 2019; 115(1): 46-56.
[http://dx.doi.org/10.1093/cvr/cvy156] [PMID: 29931225]
[45]
Strickland M, Yacoubi-Loueslati B, Bouhaouala-Zahar B, Pender SLF, Larbi A. Relationships between ion channels, mitochondrial func-tions and inflammation in human aging. Front Physiol 2019; 10: 158.
[http://dx.doi.org/10.3389/fphys.2019.00158] [PMID: 30881309]
[46]
Santulli G, Marks AR. Essential roles of intracellular calcium release channels in muscle, brain, metabolism, and aging. Curr Mol Pharmacol 2015; 8(2): 206-22.
[http://dx.doi.org/10.2174/1874467208666150507105105] [PMID: 25966694]
[47]
Rao V, Kaja S, Gentile S. Ion channels in aging and aging-related diseases In: Naofumi S, Ed Molecular mechanisms of the aging process and rejuvenation IntechOpen 2016 Available from: https://www.intechopen.com/chapters/51760
[http://dx.doi.org/10.5772/63951]
[48]
Ashrafuzzaman M, Tuszynski J. Regulation of channel function due to coupling with a lipid bilayer. J Comput Theor Nanosci 2012; 9(4): 564-70.
[http://dx.doi.org/10.1166/jctn.2012.2062]
[49]
Ashrafuzzaman M, Tuszynski JA. Membrane Biophysics. Springer-Verlag Berlin Heidelberg 2012.
[http://dx.doi.org/10.1007/978-3-642-16105-6]
[50]
Ashrafuzzaman M. Nature: Springer international publishing AG, part of springer. 2018. Nanoscale Biophysics of the Cell
[http://dx.doi.org/10.1007/978-3-319-77465-7]
[51]
Lemeshko VV. Model of the outer membrane potential generation by the inner membrane of mitochondria. Biophys J 2002; 82(2): 684-92.
[http://dx.doi.org/10.1016/S0006-3495(02)75431-3] [PMID: 11806911]
[52]
Scaduto RC Jr, Grotyohann LW. Measurement of mitochondrial membrane potential using fluorescent rhodamine derivatives. Biophys J 1999; 76(1 Pt 1): 469-77.
[http://dx.doi.org/10.1016/S0006-3495(99)77214-0] [PMID: 9876159]
[53]
Forrest MD. Why cancer cells have a more hyperpolarised mitochondrial membrane potential and emergent prospects for therapy. Bio Rxiv 2015. Available from: https://www.biorxiv.org/content/10.1101/025197v1.full
[54]
Jahangir A, Ozcan C, Holmuhamedov EL, Terzic A. Increased calcium vulnerability of senescent cardiac mitochondria: Protective role for a mitochondrial potassium channel opener. Mech Ageing Dev 2001; 122(10): 1073-86.
[http://dx.doi.org/10.1016/S0047-6374(01)00242-1] [PMID: 11389925]
[55]
Ranki HJ, Crawford RM, Budas GR. Jovanović A. Ageing is associated with a decrease in the number of sarcolemmal ATP-sensitive K+ channels in a gender-dependent manner. Mech Ageing Dev 2002; 123(6): 695-705.
[http://dx.doi.org/10.1016/S0047-6374(01)00415-8] [PMID: 11850031]
[56]
Truong AH, Murugesan S, Youssef KD, Makino A. Mitochondrial Ion channels in metabolic disease. In: Levitan PI, Dopico MDPA, Eds. vascular ion channels in physiology and disease. Cham: Springer International Publishing 2016.
[http://dx.doi.org/10.1007/978-3-319-29635-7_18]
[57]
Roscoe AK, Christensen JD, Lynch C III. Isoflurane, but not halothane, induces protection of human myocardium via adenosine A1 re-ceptors and adenosine triphosphate-sensitive potassium channels. Anesthesiology 2000; 92(6): 1692-701.
[http://dx.doi.org/10.1097/00000542-200006000-00029] [PMID: 10839921]
[58]
Kamada N, Kanaya N, Hirata N, Kimura S, Namiki A. Cardioprotective effects of propofol in isolated ischemia-reperfused guinea pig hearts: Role of KATP channels and GSK-3β Can J Anesthesia 2008; 55(9): 595-605.
[http://dx.doi.org/10.1007/BF03021433]
[59]
Demuro A, Smith M, Parker I. Single-channel Ca(2+) imaging implicates Aβ1-42 amyloid pores in Alzheimer’s disease pathology. J Cell Biol 2011; 195(3): 515-24.
[http://dx.doi.org/10.1083/jcb.201104133] [PMID: 22024165]
[60]
Alberdi E, Sánchez-Gómez MV, Cavaliere F, et al. Amyloid β oligomers induce Ca2+ dysregulation and neuronal death through activation of ionotropic glutamate receptors. Cell Calcium 2010; 47(3): 264-72.
[http://dx.doi.org/10.1016/j.ceca.2009.12.010] [PMID: 20061018]
[61]
Rostovtseva TK, Gurnev PA, Protchenko O, et al. α-Synuclein shows high affinity interaction with voltage-dependent anion channel, suggesting mechanisms of mitochondrial regulation and toxicity in parkinson disease. J Biol Chem 2015; 290(30): 18467-77.
[http://dx.doi.org/10.1074/jbc.M115.641746] [PMID: 26055708]
[62]
Ferguson M, Mockett RJ, Shen Y, Orr WC, Sohal RS. Age-associated decline in mitochondrial respiration and electron transport in Dro-sophila melanogaster. Biochem J 2005; 390(Pt 2): 501-11.
[http://dx.doi.org/10.1042/BJ20042130] [PMID: 15853766]
[63]
Rea SL, Ventura N, Johnson TE. Relationship between mitochondrial electron transport chain dysfunction, development, and life exten-sion in Caenorhabditis elegans. PLoS Biol 2007; 5(10): e259.
[http://dx.doi.org/10.1371/journal.pbio.0050259] [PMID: 17914900]
[64]
Chistiakov DA, Sobenin IA, Revin VV, Orekhov AN, Bobryshev YV. Mitochondrial aging and age-related dysfunction of mitochondria. BioMed Res Int 2014; 2014: 238463.
[http://dx.doi.org/10.1155/2014/238463] [PMID: 24818134]
[65]
Doria E, Buonocore D, Focarelli A, Marzatico F. Relationship between human aging muscle and oxidative system pathway. Oxid Med Cell Longev 2012; 2012: 1.13.
[http://dx.doi.org/10.1155/2012/830257] [PMID: 22685621]
[66]
Harman D. The free-radical theory of aging. Free Radicals Biol 1982; 255-75.
[http://dx.doi.org/10.1016/B978-0-12-566505-6.50015-6]
[67]
Harman D. Free radical theory of aging Mutation Res/DNAging 1992; 275(3-6): 257-66.
[http://dx.doi.org/10.1016/0921-8734(92)90030-S]
[68]
Peixoto PM, Kinnally KW, Pavlov E. John Wiley & Sons, Inc. 2015; pp. Mitochondrial channels in neurodegeneration. In: Valentin KG, Jonas EA, Hardwick JM, Eds. The Functions, Disease- Related Dysfunctions, and Therapeutic Targeting of Neuronal Mitochondria. John Wiley & Sons, Inc. 2015; pp. 65-100.
[http://dx.doi.org/10.1002/9781119017127.ch3]
[69]
Wang YZ, Zeng WZ, Xiao X, et al. Intracellular ASIC1a regulates mitochondrial permeability transition-dependent neuronal death. Cell Death Differ 2013; 20(10): 1359-69.
[http://dx.doi.org/10.1038/cdd.2013.90] [PMID: 23852371]
[70]
Gleichmann M, Mattson MP. Neuronal calcium homeostasis and dysregulation. Antioxid Redox Signal 2011; 14(7): 1261-73.
[http://dx.doi.org/10.1089/ars.2010.3386] [PMID: 20626318]
[71]
Williams GS, Boyman L, Chikando AC, Khairallah RJ, Lederer WJ. Mitochondrial calcium uptake. Proc Natl Acad Sci USA 2013; 110(26): 10479-86.
[http://dx.doi.org/10.1073/pnas.1300410110] [PMID: 23759742]
[72]
Perier C, Vila M. Mitochondrial biology and Parkinson’s disease. Cold Spring Harb Perspect Med 2012; 2(2): a009332.
[http://dx.doi.org/10.1101/cshperspect.a009332] [PMID: 22355801]
[73]
Zhao W, Wang J, Varghese M, et al. Impaired mitochondrial energy metabolism as a novel risk factor for selective onset and progression of dementia in oldest-old subjects. Neuropsychiatr Dis Treat 2015; 11: 565-74.
[http://dx.doi.org/10.2147/NDT.S74898] [PMID: 25784811]
[74]
Pennisi M, Lanza G, Cantone M, et al. Acetyl-l-carnitine in dementia and other cognitive disorders: A critical update. Nutrients 2020; 12(5): 1389.
[http://dx.doi.org/10.3390/nu12051389] [PMID: 32408706]
[75]
Lanza G, Cantone M, Musso S, Borgione E, Scuderi C, Ferri R. Early-onset subcortical ischemic vascular dementia in an adult with mtDNA mutation 3316G>A. J Neurol 2018; 265(4): 968-9.
[http://dx.doi.org/10.1007/s00415-018-8795-x] [PMID: 29464373]
[76]
Lanza G, Centonze SS, Destro G, et al. Shiatsu as an adjuvant therapy for depression in patients with Alzheimer’s disease: A pilot study. Complement Ther Med 2018; 38: 74-8.
[http://dx.doi.org/10.1016/j.ctim.2018.04.013] [PMID: 29857884]
[77]
Lanza G, Bella R, Cantone M, Pennisi G, Ferri R, Pennisi M. Cognitive impairment and celiac disease: Is transcranial magnetic stimulation a trait d’union between gut and brain? Int J Mol Sci 2018; 19(8): 2243.
[http://dx.doi.org/10.3390/ijms19082243] [PMID: 30065211]
[78]
Lanza G, Pino M, Fisicaro F, et al. Motor activity and Becker’s muscular dystrophy: Lights and shadows. Phys Sportsmed 2020; 48(2): 151-60.
[http://dx.doi.org/10.1080/00913847.2019.1684810] [PMID: 31646922]
[79]
Bondy SC, Yang YE, Walsh TJ, Gie YW, Lahiri DK. Dietary modulation of age-related changes in cerebral pro-oxidant status. Neurochem Int 2002; 40(2): 123-30.
[http://dx.doi.org/10.1016/S0197-0186(01)00084-5] [PMID: 11738478]
[80]
Salemi M, Cosentino F, Lanza G, et al. MRNA expression profiling of mitochondrial subunits in subjects with parkinson’s disease Arch Med Sci 2021. Available from: https://www.archivesofmedicalscience.com/pdf-131629-63360?filename=mRNA%20expression%20profiling.pdf
[http://dx.doi.org/10.5114/aoms/131629]
[81]
Pakpian N, Phopin K, Kitidee K, Govitrapong P, Wongchitrat P. Alterations in mitochondrial dynamic-related genes in the peripheral blood of alzheimer’s disease patients. Curr Alzheimer Res 2020; 17(7): 616-25.
[http://dx.doi.org/10.2174/1567205017666201006162538] [PMID: 33023448]
[82]
Cavezzi A, Ambrosini L, Colucci R, Ionna GD, Urso SU. Aging in the perspective of integrative medicine, psychoneuro endocrine immu-nology and Hormesis. Curr Aging Sci 2020; 13(2): 82-91.
[http://dx.doi.org/10.2174/1874609812666191129095417] [PMID: 31782371]
[83]
Bigland MJ, Brichta AM, Smith DW. Effects of ageing on the mitochondrial genome in rat vestibular organs. Curr Aging Sci 2018; 11(2): 108-17.
[http://dx.doi.org/10.2174/1874609811666180830143358] [PMID: 30777575]
[84]
Wu AJ, Tong BC, Huang AS, Li M, Cheung KH. Mitochondrial calcium signaling as a therapeutic target for alzheimer’s disease. Curr Alzheimer Res 2020; 17(4): 329-43.
[http://dx.doi.org/10.2174/1567205016666191210091302] [PMID: 31820698]
[85]
Jara CK, Torres AA, Olesen M, Tapia-Rojas C. Mitochondrial dysfunction as a key event during aging: from synaptic failure to memory loss In: Stavros JB, Ed Mitochondria and Brain Disorders IntechOpen 2020. Available from: https://www.intechopen.com/chapters/68488
[http://dx.doi.org/10.5772/intechopen.88445]
[86]
Mammucari C, Rizzuto R. Signaling pathways in mitochondrial dysfunction and aging. Mech Ageing Dev 2010; 131(7-8): 536-43.
[http://dx.doi.org/10.1016/j.mad.2010.07.003] [PMID: 20655326]
[87]
Akbari M, Kirkwood TBL, Bohr VA. Mitochondria in the signaling pathways that control longevity and health span Ageing Res Rev 2019. 54: 100940.
[http://dx.doi.org/10.1016/j.arr.2019.100940] [PMID: 31415807]

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