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Current Cardiology Reviews

Editor-in-Chief

ISSN (Print): 1573-403X
ISSN (Online): 1875-6557

Review Article

Myocardial Infarction as a Consequence of Mitochondrial Dysfunction

Author(s): Pranay Wal*, Namra Aziz, Yash Kumar Singh, Ankita Wal, Sourabh Kosey and Awani Kumar Rai

Volume 19, Issue 6, 2023

Published on: 12 June, 2023

Article ID: e080523216642 Pages: 8

DOI: 10.2174/1573403X19666230508114311

Price: $65

Abstract

Acute myocardial infarction is an event of myocardial necrosis caused by unstable ischemic syndrome. Myocardial infarction (MI) occurs when blood stops flowing to the cardiac tissue or myocardium and the heart muscle gets damaged due to poor perfusion and reduced oxygen supply. Mitochondria can serve as the arbiter of cell fate in response to stress. Oxidative metabolism is the function of mitochondria within the cell. Cardiac cells being highly oxidative tissue generates about 90% of their energy through oxidative metabolism. In this review, we focused on the role of mitochondria in energy generation in myocytes as well as its consequences on heart cells causing cell damage. The role of mitochondrial dysfunction due to oxidative stress, production of reactive oxygen species, and anaerobic production of lactate as a failure of oxidative metabolism are also discussed.

Keywords: Myocardial Infarction (MI), mitochondrial dysfunction, calcium overload, reactive oxygen species, cell damage, oxidative stress apoptosis.

Graphical Abstract
[1]
The top 10 causes of death. World Health Organization 2011.https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death
[2]
Kerr JFR. Shrinkage necrosis: A distinct mode of cellular death. J Pathol 1971; 105(1): 13-20.
[http://dx.doi.org/10.1002/path.1711050103] [PMID: 4108566]
[3]
Mackay J, Mensah GA. The atlas of heart disease and stroke. Geneva: WHO 2004.
[4]
Lesnefsky EJ, Moghaddas S, Tandler B, et al. Mitochondrial dysfunction in cardiac disease:Ischemia-reperfusion, aging, and heart failure. J Mol Cell Cardiol 2001; 33(6): 1065-89.
[http://dx.doi.org/10.1006/jmcc.2001.1378] [PMID: 11444914]
[5]
Mol J, Pepe S. Mitochondrial function in ischemia and reperfusion of the ageing heart. Clin Exp Pharmacol Physiol 2000; 27(9): 745-50.
[http://dx.doi.org/10.1046/j.1440-1681.2000.03326.x] [PMID: 10972544]
[6]
Kitsis RN, Peng CF, Cuervo AM. Eat your heart out. Nat Med 2007; 13(5): 539-41.
[http://dx.doi.org/10.1038/nm0507-539] [PMID: 17479097]
[7]
Matsushima S, Ide T, Yamato M, et al. Overexpression of mitochondrial peroxiredoxin-3 prevents left ventricular remodeling and failure after myocardial infarction in mice. Circulation 2006; 113(14): 1779-86.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.105.582239] [PMID: 16585391]
[8]
Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012; 60(16): 1581-98.
[http://dx.doi.org/10.1016/j.jacc.2012.08.001] [PMID: 22958960]
[9]
Eastwood JA, Johnson BD, Rutledge T, et al. Anginal symptoms, coronary artery disease, and adverse outcomes in Black and White women: The NHLBI-sponsored Women’s Ischemia Syndrome Evaluation (WISE) study. J Womens Health 2013; 22(9): 724-32.
[http://dx.doi.org/10.1089/jwh.2012.4031] [PMID: 23992103]
[10]
Ong SB, Hall AR, Hausenloy DJ. Mitochondrial dynamics in cardiovascular health and disease. Antioxid Redox Signal 2013; 19(4): 400-14.
[http://dx.doi.org/10.1089/ars.2012.4777] [PMID: 22793879]
[11]
Valensi P, Lorgis L, Cottin Y. Prevalence, incidence, predictive factors and prognosis of silent myocardial infarction: A review of the literature. Arch Cardiovasc Dis 2011; 104(3): 178-88.
[http://dx.doi.org/10.1016/j.acvd.2010.11.013] [PMID: 21497307]
[12]
Aggarwal A, Aggarwal S, Goel A, Sharma V, Dwivedi S. A retrospective 388 case-control study of modifiable risk factors and cutaneous markers in 389 Indian patients with young coronary artery disease. JRSM Cardiovasc 2012; 1: 390.
[13]
McManus DD, Piacentine SM, Lessard D, Gore JM, Yarzebski J. Thirty-year (1975 to 2005) trends in the incidence rates, clinical features, treatment practices, and short-term outcomes of patients 55 years of age hospitalized with an initial acute myocardial infarction. Am J Cardiol 2011; 108(4): 477-82.
[http://dx.doi.org/10.1016/j.amjcard.2011.03.074] [PMID: 21624538]
[14]
Incalcaterra E, Caruso M, Lo Presti R, Caimi G. Myocardial infarction in young adults: Risk factors, clinical characteristics and prognosis according to our experience. Clin Ter 2013; 164(2): e77-82.
[PMID: 23698218]
[15]
Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med 2013; 368(21): 2004-13.
[http://dx.doi.org/10.1056/NEJMra1216063] [PMID: 23697515]
[16]
Ide T, Tsutsui H, Hayashidani S, et al. Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction. Circ Res 2001; 88(5): 529-35.
[http://dx.doi.org/10.1161/01.RES.88.5.529] [PMID: 11249877]
[17]
Sahin E, Colla S, Liesa M, et al. Telomere dysfunction induces metabolic and mitochondrial compromise. Nature 2011; 470(7334): 359-65.
[http://dx.doi.org/10.1038/nature09787] [PMID: 21307849]
[18]
Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014; 129(S2): S1-S45.
[http://dx.doi.org/10.1161/01.cir.0000437738.63853.7a] [PMID: 24222016]
[19]
Sayen JJ, Sheldon WF, Peirce G, Kuo PT. Polarographic oxygen, the epicardial electrocardiogram and muscle contraction in experimental acute regional ischemia of the left ventricle. Circ Res 1958; 6(6): 779-98.
[http://dx.doi.org/10.1161/01.res.6.6.779] [PMID: 13585607]
[20]
Jennings RB. Historical perspective on the pathology of myocardial ischemia/reperfusion injury. Circ Res 2013; 113(4): 428-38.
[http://dx.doi.org/10.1161/CIRCRESAHA.113.300987] [PMID: 23908330]
[21]
Elliott AC, Smith GL, Eisner DA, Allen DG. Metabolic changes during ischaemia and their role in contractile failure in isolated ferret hearts. J Physiol 1992; 454(1): 467-90.
[http://dx.doi.org/10.1113/jphysiol.1992.sp019274] [PMID: 1474498]
[22]
Bolli R, Marbán E. Molecular and cellular mechanisms of myocardial stunning. Physiol Rev 1999; 79(2): 609-34.
[http://dx.doi.org/10.1152/physrev.1999.79.2.609] [PMID: 10221990]
[23]
Sekili S, McCay PB, Li XY, et al. Direct evidence that the hydroxyl radical plays a pathogenetic role in myocardial “stunning” in the conscious dog and demonstration that stunning can be markedly attenuated without subsequent adverse effects. Circ Res 1993; 73(4): 705-23.
[http://dx.doi.org/10.1161/01.RES.73.4.705] [PMID: 8396504]
[24]
Marín-García J, Goldenthal MJ. Mitochondrial centrality in heart failure. Heart Fail Rev 2008; 13(2): 137-50.
[http://dx.doi.org/10.1007/s10741-007-9079-1] [PMID: 18185992]
[25]
Williams RS. Mitochondrial gene expression in mammalian striated muscle. Evidence that variation in gene dosage is the major regulatory event. J Biol Chem 1986; 261(26): 12390-4.
[http://dx.doi.org/10.1016/S0021-9258(18)67252-7] [PMID: 3745193]
[26]
Suzuki S, Kaneko M, Chapman DC, Dhalla NS. Alterations in cardiac contractile proteins due to oxygen free radicals. Biochim Biophys Acta, Gen Subj 1991; 1074(1): 95-100.
[http://dx.doi.org/10.1016/0304-4165(91)90045-I] [PMID: 1646033]
[27]
Steenbergen C, Hill ML, Jennings RB. Volume regulation and plasma membrane injury in aerobic, anaerobic, and ischemic myocardium in vitro. Effects of osmotic cell swelling on plasma membrane integrity. Circ Res 1985; 57(6): 864-75.
[http://dx.doi.org/10.1161/01.RES.57.6.864] [PMID: 4064260]
[28]
Hall AR, Burke N, Dongworth RK, et al. Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction. Cell Death Dis 2016; 7(5): e2238.
[http://dx.doi.org/10.1038/cddis.2016.139] [PMID: 27228353]
[29]
Olivetti G, Quaini F, Sala R, et al. Acute myocardial infarction in humans is associated with activation of programmed myocyte cell death in the surviving portion of the heart. J Mol Cell Cardiol 1996; 28(9): 2005-16.
[http://dx.doi.org/10.1006/jmcc.1996.0193] [PMID: 8899559]
[30]
Saraste A, Pulkki K, Kallajoki M, Henriksen K, Parvinen M, Voipio-Pulkki LM. Apoptosis in human acute myocardial infarction. Circulation 1997; 95(2): 320-3.
[http://dx.doi.org/10.1161/01.CIR.95.2.320] [PMID: 9008443]
[31]
Narula J, Haider N, Virmani R, et al. Apoptosis in myocytes in end-stage heart failure. N Engl J Med 1996; 335(16): 1182-9.
[http://dx.doi.org/10.1056/NEJM199610173351603] [PMID: 8815940]
[32]
Aharinejad S, Andrukhova O, Lucas T, et al. Programmed cell death in idiopathic dilated cardiomyopathy is mediated by suppression of the apoptosis inhibitor Apollon. Ann Thorac Surg 2008; 86(1): 109-14.
[http://dx.doi.org/10.1016/j.athoracsur.2008.03.057] [PMID: 18573408]
[33]
Grover GJ, Atwal KS, Sleph PG, et al. Excessive ATP hydrolysis in ischemic myocardium by mitochondrial F 1 F 0 -ATPase: Effect of selective pharmacological inhibition of mitochondrial ATPase hydrolase activity. Am J Physiol Heart Circ Physiol 2004; 287(4): H1747-55.
[http://dx.doi.org/10.1152/ajpheart.01019.2003] [PMID: 15371268]
[34]
Halkos ME, Kerendi F, Corvera JS, et al. Myocardial protection with postconditioning is not enhanced by ischemic preconditioning. Ann Thorac Surg 2004; 78(3): 961-9.
[http://dx.doi.org/10.1016/j.athoracsur.2004.03.033] [PMID: 15337028]
[35]
Weisleder N, Taffet GE, Capetanaki Y. Bcl-2 overexpression corrects mitochondrial defects and ameliorates inherited desmin null cardiomyopathy. Proc Natl Acad Sci USA 2004; 101(3): 769-74.
[http://dx.doi.org/10.1073/pnas.0303202101] [PMID: 14715896]
[36]
Baines CP. The mitochondrial permeability transition pore and ischemia-reperfusion injury. Basic Res Cardiol 2009; 104(2): 181-8.
[http://dx.doi.org/10.1007/s00395-009-0004-8] [PMID: 19242640]
[37]
Di Lisa F, Bernardi P. A CaPful of mechanisms regulating the mitochondrial permeability transition. J Mol Cell Cardiol 2009; 46(6): 775-80.
[http://dx.doi.org/10.1016/j.yjmcc.2009.03.006] [PMID: 19303419]
[38]
Cellier L, Tamareille S, Kalakech H, et al. Remote ischemic conditioning influences mitochondrial dynamics. Shock 2016; 45(2): 192-7.
[http://dx.doi.org/10.1097/SHK.0000000000000500] [PMID: 26555744]
[39]
Dong Y, Undyala VVR, Przyklenk K. Inhibition of mitochondrial fission as a molecular target for cardioprotection: Critical importance of the timing of treatment. Basic Res Cardiol 2016; 111(5): 59-76.
[http://dx.doi.org/10.1007/s00395-016-0578-x] [PMID: 27573530]
[40]
Webster KA. Mitochondrial membrane permeabilization and cell death during myocardial infarction: Roles of calcium and reactive oxygen species. Future Cardiol 2012; 8(6): 863-84.
[http://dx.doi.org/10.2217/fca.12.58] [PMID: 23176689]
[41]
Din S, Mason M, Völkers M, et al. Pim-1 preserves mitochondrial morphology by inhibiting dynamin-related protein 1 translocation. Proc Natl Acad Sci 2013; 110(15): 5969-74.
[http://dx.doi.org/10.1073/pnas.1213294110] [PMID: 23530233]
[42]
Wang K, Liu C-Y, Zhang X-J, et al. miR-361-regulated prohibitin inhibits mitochondrial fission and apoptosis and protects heart from ischemia injury. Cell Death Differ 2015; 22(6): 1058-68.
[http://dx.doi.org/10.1038/cdd.2014.200] [PMID: 25501599]
[43]
Kübler W, Spieckermann PG. Regulation of glycolysis in the ischemic and the anoxic myocardium. J Mol Cell Cardiol 1970; 1(4): 351-77.
[http://dx.doi.org/10.1016/0022-2828(70)90034-9] [PMID: 4937794]
[44]
Karmazyn M, Moffat MP. Role of Na+/H+ exchange in cardiac physiology and pathophysiology: Mediation of myocardial reperfusion injury by the pH paradox. Cardiovasc Res 1993; 27(6): 915-24.
[http://dx.doi.org/10.1093/cvr/27.6.915] [PMID: 8221779]
[45]
Zhu L, Yu Y, Chua BHL, Ho YS, Kuo TH. Regulation of sodium-calcium exchange and mitochondrial energetics by Bcl-2 in the heart of transgenic mice. J Mol Cell Cardiol 2001; 33(12): 2135-44.
[http://dx.doi.org/10.1006/jmcc.2001.1476] [PMID: 11735260]
[46]
Neely JR Jr, Rovetto MJ, Whitmer JT, Morgan HE. Effects of ischemia on function and metabolism of the isolated working rat heart. Am J Physiol 1973; 225(3): 651-8.
[http://dx.doi.org/10.1152/ajplegacy.1973.225.3.651] [PMID: 4726499]
[47]
Lopaschuk GD, Belke DD, Gamble J, Toshiyuki I, Schönekess BO. Regulation of fatty acid oxidation in the mammalian heart in health and disease. Biochim Biophys Acta Lipids Lipid Metab 1994; 1213(3): 263-76.
[http://dx.doi.org/10.1016/0005-2760(94)00082-4] [PMID: 8049240]
[48]
Allard MF, Schönekess BO, Henning SL, English DR, Lopaschuk GD. Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts. Am J Physiol 1994; 267(2 Pt 2): H742-50.
[PMID: 8067430]
[49]
Ziegler DM. Role of reversible oxidation-reduction of enzyme thiols-disulfides in metabolic regulation. Annu Rev Biochem 1985; 54(1): 305-29.
[http://dx.doi.org/10.1146/annurev.bi.54.070185.001513] [PMID: 2862840]
[50]
Ceconi C, Bernocchi P, Boraso A, et al. New insights on myocardial pyridine nucleotides and thiol redox state in ischemia and reperfusion damage. Cardiovasc Res 2000; 47(3): 586-94.
[http://dx.doi.org/10.1016/S0008-6363(00)00104-8] [PMID: 10963731]
[51]
Rouslin W, Erickson JL, Solaro RJ. Effects of oligomycin and acidosis on rates of ATP depletion in ischemic heart muscle. Am J Physiol 1986; 250(3 Pt 2): H503-8.
[PMID: 2937313]
[52]
Schweichel JU, Merker HJ. The morphology of various types of cell death in prenatal tissues. Teratology 1973; 7(3): 253-66.
[http://dx.doi.org/10.1002/tera.1420070306] [PMID: 4807128]
[53]
Braasch W, Gudbjarnason S, Puri PS, Ravens KG, Bing RJ. Early changes in energy metabolism in the myocardium following acute coronary artery occlusion in anesthetized dogs. Circ Res 1968; 23(3): 429-38.
[http://dx.doi.org/10.1161/01.RES.23.3.429] [PMID: 5676453]
[54]
Ha SJ, Kim W. Mechanism of ischemia and reperfusion injury to the heart: From the viewpoint of nitric oxide and mitochondria. Chonnam Uidae Chapchi 2010; 46(3): 129-39.
[http://dx.doi.org/10.4068/cmj.2010.46.3.129]
[55]
Ong SB, Hausenloy DJ. Mitochondrial morphology and cardiovascular disease. Cardiovasc Res 2010; 88(1): 16-29.
[http://dx.doi.org/10.1093/cvr/cvq237] [PMID: 20631158]
[56]
Chan DC. Fusion and fission: Interlinked processes critical for mitochondrial health. Annu Rev Genet 2012; 46(1): 265-87.
[http://dx.doi.org/10.1146/annurev-genet-110410-132529] [PMID: 22934639]
[57]
Westermann B. Bioenergetic role of mitochondrial fusion and fission. Biochim Biophys Acta Bioenerg 2012; 1817(10): 1833-8.
[http://dx.doi.org/10.1016/j.bbabio.2012.02.033] [PMID: 22409868]
[58]
Gwechenberger M, Mendoza LH, Youker KA, et al. Cardiac myocytes produce interleukin-6 in culture and in viable border zone of reperfused infarctions. Circulation 1999; 99(4): 546-51.
[http://dx.doi.org/10.1161/01.CIR.99.4.546] [PMID: 9927402]
[59]
Dobson GP, Himmelreich U. Heart design: Free ADP scales with absolute mitochondrial and myofibrillar volumes from mouse to human. Biochim Biophys Acta Bioenerg 2002; 1553(3): 261-7.
[http://dx.doi.org/10.1016/S0005-2728(01)00247-X] [PMID: 11997135]
[60]
Maack C, O’Rourke B. Excitation-contraction coupling and mitochondrial energetics. Basic Res Cardiol 2007; 102(5): 369-92.
[http://dx.doi.org/10.1007/s00395-007-0666-z] [PMID: 17657400]
[61]
Stanley WC. Cardiac energetics during ischaemia and the rationale for metabolic interventions. Coron Artery Dis 2001; 12(S1): S3-7.
[PMID: 11286306]
[62]
Fridovich I. Superoxide radical and superoxide dismutases. Annu Rev Biochem 1995; 64(1): 97-112.
[http://dx.doi.org/10.1146/annurev.bi.64.070195.000525] [PMID: 7574505]
[63]
Maloney PC. Energy coupling to ATP synthesis by the proton-translocating ATPase. J Membr Biol 1982; 67(1): 1-12.
[http://dx.doi.org/10.1007/BF01868643] [PMID: 6178829]
[64]
Piper H, Kasseckert S, Abdallah Y. The sarcoplasmic reticulum as the primary target of reperfusion protection. Cardiovasc Res 2006; 70(2): 170-3.
[http://dx.doi.org/10.1016/j.cardiores.2006.03.010] [PMID: 16600194]
[65]
Varadarajan SG, An J, Novalija E, Smart SC, Stowe DF. Changes in [Na+], compartmental [Ca 2+], and NADH with dysfunction after global ischemia in intact hearts. Am J Physiol Heart Circ Physiol 2001; 280(1): H280-93.
[http://dx.doi.org/10.1152/ajpheart.2001.280.1.H280] [PMID: 11123243]
[66]
Gustafsson ÅB, Tsai JG, Logue SE, Crow MT, Gottlieb RA. Apoptosis repressor with caspase recruitment domain protects against cell death by interfering with Bax activation. J Biol Chem 2004; 279(20): 21233-8.
[http://dx.doi.org/10.1074/jbc.M400695200] [PMID: 15004034]
[67]
Reggiori F, Klionsky DJ. Autophagosomes: Biogenesis from scratch? Curr Opin Cell Biol 2005; 17(4): 415-22.
[http://dx.doi.org/10.1016/j.ceb.2005.06.007] [PMID: 15978794]
[68]
Griffiths EJ, Halestrap AP. Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion. Biochem J 1995; 307(1): 93-8.
[http://dx.doi.org/10.1042/bj3070093] [PMID: 7717999]
[69]
Searle J, Kerr JF, Bishop CJ. Necrosis and apoptosis: Distinct modes of cell death with fundamentally different significance. Pathol Annu 1982; 17(Pt 2): 229-59.
[PMID: 7182752]
[70]
Majno G, Joris I. Apoptosis, oncosis, and necrosis. An overview of cell death. Am J Pathol 1995; 146(1): 3-15.
[PMID: 7856735]
[71]
Danial NN, Korsmeyer SJ. Cell Death. Cell 2004; 116(2): 205-19.
[http://dx.doi.org/10.1016/S0092-8674(04)00046-7] [PMID: 14744432]
[72]
Huang DCS, Strasser A. BH3-Only proteins-essential initiators of apoptotic cell death. Cell 2000; 103(6): 839-42.
[http://dx.doi.org/10.1016/S0092-8674(00)00187-2] [PMID: 11136969]

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