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ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

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Review Article

A Mitochondrial Approach to Cardiovascular Risk and Disease

Author(s): Caroline D. Veloso, Getachew D. Belew, Luciana L. Ferreira, Luís F. Grilo, John G. Jones, Piero Portincasa, Vilma A. Sardão and Paulo J. Oliveira*

Volume 25, Issue 29, 2019

Page: [3175 - 3194] Pages: 20

DOI: 10.2174/1389203720666190830163735

Price: $65

Abstract

Background: Cardiovascular diseases (CVDs) are a leading risk factor for mortality worldwide and the number of CVDs victims is predicted to rise through 2030. While several external parameters (genetic, behavioral, environmental and physiological) contribute to cardiovascular morbidity and mortality; intrinsic metabolic and functional determinants such as insulin resistance, hyperglycemia, inflammation, high blood pressure and dyslipidemia are considered to be dominant factors.

Methods: Pubmed searches were performed using different keywords related with mitochondria and cardiovascular disease and risk. In vitro, animal and human results were extracted from the hits obtained.

Results: High cardiac energy demand is sustained by mitochondrial ATP production, and abnormal mitochondrial function has been associated with several lifestyle- and aging-related pathologies in the developed world such as diabetes, non-alcoholic fatty liver disease (NAFLD) and kidney diseases, that in turn can lead to cardiac injury. In order to delay cardiac mitochondrial dysfunction in the context of cardiovascular risk, regular physical activity has been shown to improve mitochondrial parameters and myocardial tolerance to ischemia-reperfusion (IR). Furthermore, pharmacological interventions can prevent the risk of CVDs. Therapeutic agents that can target mitochondria, decreasing ROS production and improve its function have been intensively researched. One example is the mitochondria-targeted antioxidant MitoQ10, which already showed beneficial effects in hypertensive rat models. Carvedilol or antidiabetic drugs also showed protective effects by preventing cardiac mitochondrial oxidative damage.

Conclusion: This review highlights the role of mitochondrial dysfunction in CVDs, also show-casing several approaches that act by improving mitochondrial function in the heart, contributing to decrease some of the risk factors associated with CVDs.

Keywords: Mitochondria, Cardiovascular diseases, metabolism, mitochondrial dysfunction, cardiovascular risk, insulin resistance.

« Previous
[1]
World Health Organization. Global health estimates: deaths and causes, age, sex and country 2014.
[2]
Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: Analysis of worldwide data. Lancet 2005; 365(9455): 217-23.
[http://dx.doi.org/10.1016/S0140-6736(05)17741-1] [PMID: 15652604]
[3]
Celermajer DS, Chow CK, Marijon E, Anstey NM, Woo KS. Cardiovascular disease in the developing world: Prevalences, patterns, and the potential of early disease detection. J Am Coll Cardiol 2012; 60(14): 1207-16.
[http://dx.doi.org/10.1016/j.jacc.2012.03.074] [PMID: 22858388]
[4]
Mathers CD, Salomon JA, Ezzati M, Begg S, Vander Hoorn S, Lopez AD. Sensitivity and uncertainty analyses for burden of disease and risk factor estimates. In: Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJL, Eds. Global Burden of Disease and Risk Factors. Washington, DC: World Bank 2006. Chapter 5.
[5]
Dzau VJ, Antman EM, Black HR, et al. The cardiovascular disease continuum validated: Clinical evidence of improved patient outcomes: Part I: Pathophysiology and clinical trial evidence (risk factors through stable coronary artery disease). Circulation 2006; 114(25): 2850-70.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.106.655688] [PMID: 17179034]
[6]
Ezzati M, Vander Hoorn S, Lawes CMM, et al. Rethinking the “diseases of affluence” paradigm: Global patterns of nutritional risks in relation to economic development. PLoS Med 2005; 2(5)e133
[7]
Dahlöf B. Cardiovascular disease risk factors: Epidemiology and risk assessment. Am J Cardiol 2010; 105(1)(Suppl.): 3A-9A.
[http://dx.doi.org/10.1016/j.amjcard.2009.10.007] [PMID: 20102968]
[8]
De Backer G. Epidemiology and prevention of cardiovascular disease: Quo vadis? Eur J Prev Cardiol 2017; 24(7): 768-72.
[9]
Balakumar P, Maung UK, Jagadeesh G. Prevalence and prevention of cardiovascular disease and diabetes mellitus. Pharmacol Res 2016; 113(Pt A): 600-9.
[http://dx.doi.org/10.1016/j.phrs.2016.09.040] [PMID: 27697647]
[10]
Tzoulaki I, Elliott P, Kontis V, Ezzati M. Worldwide exposures to cardiovascular risk factors and associated health effects: Current knowledge and data gaps. Circulation 2016; 133(23): 2314-33.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.115.008718] [PMID: 27267538]
[11]
Ezzati M, Hoorn SV, Rodgers A, et al. Estimates of global and regional potential health gains from reducing multiple major risk factors. Lancet 2003; 362(9380): 271-80.
[http://dx.doi.org/10.1016/S0140-6736(03)13968-2] [PMID: 12892956]
[12]
Mahmood SS, Levy D, Vasan RS, Wang TJ. The Framingham Heart Study and the epidemiology of cardiovascular disease: A historical perspective. Lancet 2014; 383(9921): 999-1008.
[http://dx.doi.org/10.1016/S0140-6736(13)61752-3] [PMID: 24084292]
[13]
Appelman Y, van Rijn BB, Ten Haaf ME, Boersma E, Peters SAE. Sex differences in cardiovascular risk factors and disease prevention. Atherosclerosis 2015; 241(1): 211-8.
[http://dx.doi.org/10.1016/j.atherosclerosis.2015.01.027] [PMID: 25670232]
[14]
Pucci G, Alcidi R, Tap L, Battista F, Mattace-Raso F, Schillaci G. Sex- and gender-related prevalence, cardiovascular risk and therapeutic approach in metabolic syndrome: A review of the literature. Pharmacol Res 2017; 120: 34-42.
[http://dx.doi.org/10.1016/j.phrs.2017.03.008] [PMID: 28300617]
[15]
Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA 2003; 289(1): 76-9.
[http://dx.doi.org/10.1001/jama.289.1.76] [PMID: 12503980]
[16]
Finucane MM, Stevens GA, Cowan MJ, et al. National, regional, and global trends in body-mass index since 1980: Systematic analysis of health examination surveys and epidemiological studies with 960 country-years and 9·1 million participants. Lancet 2011; 377(9765): 557-67.
[http://dx.doi.org/10.1016/S0140-6736(10)62037-5] [PMID: 21295846]
[17]
World Health Organization. Obesity and overweight 2018.
[18]
Ford ES. Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: A summary of the evidence. Diabetes Care 2005; 28(7): 1769-78.
[http://dx.doi.org/10.2337/diacare.28.7.1769] [PMID: 15983333]
[19]
Ioannidis JPA. Implausible results in human nutrition research. BMJ 2013; 347: f6698.
[http://dx.doi.org/10.1136/bmj.f6698] [PMID: 24231028]
[20]
Burdge GC, Lillycrop KA, Jackson AA. Nutrition in early life, and risk of cancer and metabolic disease: Alternative endings in an epigenetic tale? Br J Nutr 2009; 101(5): 619-30.
[http://dx.doi.org/10.1017/S0007114508145883] [PMID: 19079817]
[21]
Menendez-Castro C, Rascher W, Hartner A. Intrauterine growth restriction - impact on cardiovascular diseases later in life. Mol Cell Pediatr 2018; 5(1): 4.
[http://dx.doi.org/10.1186/s40348-018-0082-5] [PMID: 29560535]
[22]
Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. BMJ 2014; 349: g4164.
[http://dx.doi.org/10.1136/bmj.g4164] [PMID: 25011450]
[23]
World Health Organization. Global status report on Alcohol and Health 2014.
[24]
Lim SS, Vos T, Flaxman AD, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012; 380(9859): 2224-60.
[http://dx.doi.org/10.1016/S0140-6736(12)61766-8] [PMID: 23245609]
[25]
Sattelmair J, Pertman J, Ding EL, Kohl HW III, Haskell W, Lee IM. Dose response between physical activity and risk of coronary heart disease: A meta-analysis. Circulation 2011; 124(7): 789-95.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.110.010710] [PMID: 21810663]
[26]
Löllgen H, Böckenhoff A, Knapp G. Physical activity and all-cause mortality: An updated meta-analysis with different intensity categories. Int J Sports Med 2009; 30(3): 213-24.
[27]
Fletcher GF, Balady G, Blair SN, et al. Statement on exercise: Benefits and recommendations for physical activity programs for all Americans. A statement for health professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology, American Heart Association. Circulation 1996; 94(4): 857-62.
[http://dx.doi.org/10.1161/01.CIR.94.4.857] [PMID: 8772712]
[28]
Gottlieb DJ, Redline S, Nieto FJ, et al. Association of usual sleep duration with hypertension: The sleep heart health study. Sleep 2006; 29(8): 1009-14.
[http://dx.doi.org/10.1093/sleep/29.8.1009] [PMID: 16944668]
[29]
Wolk R, Somers VK. Sleep and the metabolic syndrome. Exp Physiol 2007; 92(1): 67-78.
[http://dx.doi.org/10.1113/expphysiol.2006.033787] [PMID: 17085678]
[30]
Brook RD, Rajagopalan S, Pope CA III, et al. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation 2010; 121(21): 2331-78.
[http://dx.doi.org/10.1161/CIR.0b013e3181dbece1] [PMID: 20458016]
[31]
Di Ciaula A, Portincasa P. Diet and contaminants: Driving the rise to obesity epidemics? Curr Med Chem 2017. In Press
[http://dx.doi.org/10.2174/0929867324666170518095736] [PMID: 28521687]
[32]
Kontis V, Mathers CD, Rehm J, et al. Contribution of six risk factors to achieving the 25×25 non-communicable disease mortality reduction target: A modelling study. Lancet 2014; 384(9941): 427-37.
[http://dx.doi.org/10.1016/S0140-6736(14)60616-4] [PMID: 24797573]
[33]
Ormazabal V, Nair S, Elfeky O, Aguayo C, Salomon C, Zuñiga FA. Association between insulin resistance and the development of cardiovascular disease. Cardiovasc Diabetol 2018; 17(1): 122.
[http://dx.doi.org/10.1186/s12933-018-0762-4] [PMID: 30170598]
[34]
Bonora E, Kiechl S, Willeit J, et al. Prevalence of insulin resistance in metabolic disorders: The Bruneck Study. Diabetes 1998; 47(10): 1643-9.
[http://dx.doi.org/10.2337/diabetes.47.10.1643] [PMID: 9753305]
[35]
Howard G, O’Leary DH, Zaccaro D, et al. Insulin sensitivity and atherosclerosis. Circulation 1996; 93(10): 1809-17.
[http://dx.doi.org/10.1161/01.CIR.93.10.1809] [PMID: 8635260]
[36]
Tenenbaum A, Adler Y, Boyko V, et al. Insulin resistance is associated with increased risk of major cardiovascular events in patients with preexisting coronary artery disease. Am Heart J 2007; 153(4): 559-65.
[http://dx.doi.org/10.1016/j.ahj.2007.01.008] [PMID: 17383294]
[37]
Gast KB, Tjeerdema N, Stijnen T, Smit JWA, Dekkers OM. Insulin resistance and risk of incident cardiovascular events in adults without diabetes: Meta-analysis. PLoS One 2012; 7(12)e52036
[http://dx.doi.org/10.1371/journal.pone.0052036] [PMID: 23300589]
[38]
Eddy D, Schlessinger L, Kahn R, Peskin B, Schiebinger R. Relationship of insulin resistance and related metabolic variables to coronary artery disease: A mathematical analysis. Diabetes Care 2009; 32(2): 361-6.
[http://dx.doi.org/10.2337/dc08-0854] [PMID: 19017770]
[39]
Reaven G. Insulin resistance and coronary heart disease in nondiabetic individuals. Arterioscler Thromb Vasc Biol 2012; 32(8): 1754-9.
[http://dx.doi.org/10.1161/ATVBAHA.111.241885] [PMID: 22815340]
[40]
Laakso M, Kuusisto J. Insulin resistance and hyperglycaemia in cardiovascular disease development. Nat Rev Endocrinol 2014; 10(5): 293-302.
[http://dx.doi.org/10.1038/nrendo.2014.29] [PMID: 24663222]
[41]
Rader DJ. Effect of insulin resistance, dyslipidemia, and intra-abdominal adiposity on the development of cardiovascular disease and diabetes mellitus. Am J Med 2007; 120(3)(Suppl. 1): S12-8.
[http://dx.doi.org/10.1016/j.amjmed.2007.01.003] [PMID: 17320517]
[42]
Savaiano DA, Story JA. Cardiovascular disease and fiber: Is insulin resistance the missing link? Nutr Rev 2000; 58(11): 356-8.
[http://dx.doi.org/10.1111/j.1753-4887.2000.tb01834.x] [PMID: 11140908]
[43]
Kong C, Elatrozy T, Anyaoku V, Robinson S, Richmond W, Elkeles RS. Insulin resistance, cardiovascular risk factors and ultrasonically measured early arterial disease in normotensive Type 2 diabetic subjects. Diabetes Metab Res Rev 2000; 16(6): 448-53.
[http://dx.doi.org/10.1002/1520-7560(2000)9999:9999<:AID-DMRR154>3.0.CO;2-N]
[44]
Ginsberg HN. Insulin resistance and cardiovascular disease. J Clin Invest 2000; 106(4): 453-8.
[http://dx.doi.org/10.1172/JCI10762] [PMID: 10953019]
[45]
Bloomgarden ZT. Insulin resistance, dyslipidemia, and cardiovascular disease. Diabetes Care 2007; 30(8): 2164-70.
[http://dx.doi.org/10.2337/dc07-zb08] [PMID: 17855278]
[46]
Kozakova M, Natali A, Dekker J, et al. Insulin sensitivity and carotid intima-media thickness: Relationship between insulin sensitivity and cardiovascular risk study. Arterioscler Thromb Vasc Biol 2013; 33(6): 1409-17.
[http://dx.doi.org/10.1161/ATVBAHA.112.300948] [PMID: 23599442]
[47]
Bornfeldt KE, Tabas I. Insulin resistance, hyperglycemia, and atherosclerosis. Cell Metab 2011; 14(5): 575-85.
[http://dx.doi.org/10.1016/j.cmet.2011.07.015] [PMID: 22055501]
[48]
Davidson JA, Parkin CG. Is hyperglycemia a causal factor in cardiovascular disease? Does proving this relationship really matter? Yes Diabetes Care 2009; 32(2): S331-3.
[http://dx.doi.org/10.2337/dc09-S333]
[49]
Chanda D, Luiken JJFP, Glatz JFC. Signaling pathways involved in cardiac energy metabolism. FEBS Lett 2016; 590(15): 2364-74.
[http://dx.doi.org/10.1002/1873-3468.12297] [PMID: 27403883]
[50]
Zhou YT, Grayburn P, Karim A, et al. Lipotoxic heart disease in obese rats: Implications for human obesity. Proc Natl Acad Sci USA 2000; 97(4): 1784-9.
[http://dx.doi.org/10.1073/pnas.97.4.1784] [PMID: 10677535]
[51]
Wu G, Meininger CJ. Nitric oxide and vascular insulin resistance. Biofactors 2009; 35(1): 21-7.
[http://dx.doi.org/10.1002/biof.3] [PMID: 19319842]
[52]
Wang CCL, Gurevich I, Draznin B. Insulin affects vascular smooth muscle cell phenotype and migration via distinct signaling pathways. Diabetes 2003; 52(10): 2562-9.
[http://dx.doi.org/10.2337/diabetes.52.10.2562] [PMID: 14514641]
[53]
Dinesh Shah A, Langenberg C, Rapsomaniki E, et al. Type 2 diabetes and incidence of a wide range of cardiovascular diseases: A cohort study in 1.9 million people. Lancet 2015; 385(Suppl. 1): S86.
[http://dx.doi.org/10.1016/S0140-6736(15)60401-9] [PMID: 26312908]
[54]
Martín-Timón I, Sevillano-Collantes C, Segura-Galindo A, Del Cañizo-Gómez FJ. Type 2 diabetes and cardiovascular disease: Have all risk factors the same strength? World J Diabetes 2014; 5(4): 444-70.
[http://dx.doi.org/10.4239/wjd.v5.i4.444] [PMID: 25126392]
[55]
Ciccone MM, Cortese F, Gesualdo M, Donvito I, Carbonara S, De Pergola G. A glycemic threshold of 90 mg/dl promotes early signs of atherosclerosis in apparetly healthy overweight/obese subjects. Endocr Metab Immune Disord Drug Targets 2016; 16(4): 288-95.
[http://dx.doi.org/10.2174/1871530317666161205124955] [PMID: 27919218]
[56]
Meyer ML, Gotman NM, Soliman EZ, et al. Association of glucose homeostasis measures with heart rate variability among Hispanic/Latino adults without diabetes: The Hispanic Community Health Study/Study of Latinos (HCHS/SOL). Cardiovasc Diabetol 2016; 15: 45.
[http://dx.doi.org/10.1186/s12933-016-0364-y] [PMID: 26983644]
[57]
Paneni F, Volpe M, Lüscher TF, Cosentino F. SIRT1, p66(Shc), and Set7/9 in vascular hyperglycemic memory: Bringing all the strands together. Diabetes 2013; 62(6): 1800-7.
[http://dx.doi.org/10.2337/db12-1648] [PMID: 23704521]
[58]
Ceriello A. The emerging challenge in diabetes: The “metabolic memory”. Vascul Pharmacol 2012; 57(5-6): 133-8.
[http://dx.doi.org/10.1016/j.vph.2012.05.005] [PMID: 22609133]
[59]
Fiorentino TV, Prioletta A, Zuo P, Folli F. Hyperglycemia-induced oxidative stress and its role in diabetes mellitus related cardiovascular diseases. Curr Pharm Des 2013; 19(32): 5695-703.
[http://dx.doi.org/10.2174/1381612811319320005] [PMID: 23448484]
[60]
Pistrosch F, Natali A, Hanefeld M. Is hyperglycemia a cardiovascular risk factor? Diabetes Care 2011; 34(Suppl. 2): S128-31.
[http://dx.doi.org/10.2337/dc11-s207] [PMID: 21525443]
[61]
Nowotny K, Jung T, Höhn A, Weber D, Grune T. Advanced glycation end products and oxidative stress in type 2 diabetes mellitus. Biomolecules 2015; 5(1): 194-222.
[http://dx.doi.org/10.3390/biom5010194] [PMID: 25786107]
[62]
Yan SF, Ramasamy R, Schmidt AM. The RAGE axis: A fundamental mechanism signaling danger to the vulnerable vasculature. Circ Res 2010; 106(5): 842-53.
[http://dx.doi.org/10.1161/CIRCRESAHA.109.212217] [PMID: 20299674]
[63]
Goldberg IJ. Clinical review 124: Diabetic dyslipidemia: Causes and consequences. J Clin Endocrinol Metab 2001; 86(3): 965-71.
[http://dx.doi.org/10.1210/jcem.86.3.7304] [PMID: 11238470]
[64]
Miller M. Dyslipidemia and cardiovascular risk: The importance of early prevention. QJM 2009; 102(9): 657-67.
[http://dx.doi.org/10.1093/qjmed/hcp065] [PMID: 19498039]
[65]
Sparks JD, Sparks CE, Adeli K. Selective hepatic insulin resistance, VLDL overproduction, and hypertriglyceridemia. Arterioscler Thromb Vasc Biol 2012; 32(9): 2104-12.
[http://dx.doi.org/10.1161/ATVBAHA.111.241463] [PMID: 22796579]
[66]
Austin MA, Hokanson JE, Edwards KL. Hypertriglyceridemia as a cardiovascular risk factor. Am J Cardiol 1998; 81(4A): 7B-12B.
[http://dx.doi.org/10.1016/S0002-9149(98)00031-9] [PMID: 9526807]
[67]
Hokanson JE. Hypertriglyceridemia and risk of coronary heart disease. Curr Cardiol Rep 2002; 4(6): 488-93.
[http://dx.doi.org/10.1007/s11886-002-0112-7] [PMID: 12379171]
[68]
Wende AR, Abel ED. Lipotoxicity in the heart. Biochim Biophys Acta 2010; 1801(3): 311-9.
[http://dx.doi.org/10.1016/j.bbalip.2009.09.023] [PMID: 19818871]
[69]
Mei Y, Thompson MD, Cohen RA, Tong X. Endoplasmic reticulum stress and related pathological processes. J Pharmacol Biomed Anal 2013; 1(2)1000107
[PMID: 24611136]
[70]
Taddeo EP, Laker RC, Breen DS, et al. Opening of the mitochondrial permeability transition pore links mitochondrial dysfunction to insulin resistance in skeletal muscle. Mol Metab 2013; 3(2): 124-34.
[http://dx.doi.org/10.1016/j.molmet.2013.11.003] [PMID: 24634818]
[71]
Mandavia CH, Aroor AR, Demarco VG, Sowers JR. Molecular and metabolic mechanisms of cardiac dysfunction in diabetes. Life Sci 2013; 92(11): 601-8.
[http://dx.doi.org/10.1016/j.lfs.2012.10.028] [PMID: 23147391]
[72]
Peña-Blanco A, García-Sáez AJ. Bax, Bak and beyond- mitochondrial performance in apoptosis. FEBS J 2018; 285(3): 416-31.
[http://dx.doi.org/10.1111/febs.14186] [PMID: 28755482]
[73]
Bhola PD, Letai A. Mitochondria-judges and executioners of cell death sentences. Mol Cell 2016; 61(5): 695-704.
[http://dx.doi.org/10.1016/j.molcel.2016.02.019] [PMID: 26942674]
[74]
Matilainen O, Quirós PM, Auwerx J. Mitochondria and epigenetics - crosstalk in homeostasis and stress. Trends Cell Biol 2017; 27(6): 453-63.
[http://dx.doi.org/10.1016/j.tcb.2017.02.004] [PMID: 28274652]
[75]
Cogliati S, Enriquez JA, Scorrano L. Mitochondrial cristae: Where beauty meets functionality. Trends Biochem Sci 2016; 41(3): 261-73.
[http://dx.doi.org/10.1016/j.tibs.2016.01.001] [PMID: 26857402]
[76]
Friedman JR, Nunnari J. Mitochondrial form and function. Nature 2014; 505(7483): 335-43.
[http://dx.doi.org/10.1038/nature12985] [PMID: 24429632]
[77]
Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab 2015; 21(3): 443-54.
[http://dx.doi.org/10.1016/j.cmet.2015.02.009] [PMID: 25738459]
[78]
Lee C, Yen K, Cohen P. Humanin: A harbinger of mitochondrial-derived peptides? Trends Endocrinol Metab 2013; 24(5): 222-8.
[http://dx.doi.org/10.1016/j.tem.2013.01.005] [PMID: 23402768]
[79]
Schorr S, van der Laan M. Integrative functions of the mitochondrial contact site and cristae organizing system. Semin Cell Dev Biol 2018; 76: 191-200.
[http://dx.doi.org/10.1016/j.semcdb.2017.09.021] [PMID: 28923515]
[80]
Stock D, Leslie AG, Walker JE. Molecular architecture of the rotary motor in ATP synthase. Science 1999; 286(5445): 1700-5.
[http://dx.doi.org/10.1126/science.286.5445.1700] [PMID: 10576729]
[81]
Kim HD, Kim CH, Rah BJ, Chung HI, Shim TS. Quantitative study on the relation between structural and functional properties of the hearts from three different mammals. Anat Rec 1994; 238(2): 199-206.
[http://dx.doi.org/10.1002/ar.1092380206] [PMID: 8154606]
[82]
Barth E, Stämmler G, Speiser B, Schaper J. Ultrastructural quantitation of mitochondria and myofilaments in cardiac muscle from 10 different animal species including man. J Mol Cell Cardiol 1992; 24(7): 669-81.
[http://dx.doi.org/10.1016/0022-2828(92)93381-S] [PMID: 1404407]
[83]
Balaban RS. Cardiac energy metabolism homeostasis: Role of cytosolic calcium. J Mol Cell Cardiol 2002; 34(10): 1259-71.
[http://dx.doi.org/10.1006/jmcc.2002.2082] [PMID: 12392982]
[84]
Harris DA, Das AM. Control of mitochondrial ATP synthesis in the heart. Biochem 1991; 15;280(Pt 3): 561-73.
[http://dx.doi.org/10.1042/bj2800561]
[85]
Kolwicz SC Jr, Purohit S, Tian R. Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes. Circ Res 2013; 113(5): 603-16.
[http://dx.doi.org/10.1161/CIRCRESAHA.113.302095] [PMID: 23948585]
[86]
Stanley WC, Recchia FA, Lopaschuk GD. Myocardial substrate metabolism in the normal and failing heart. Physiol Rev 2005; 85(3): 1093-129.
[http://dx.doi.org/10.1152/physrev.00006.2004] [PMID: 15987803]
[87]
Wentz AE, d’Avignon DA, Weber ML, et al. Adaptation of myocardial substrate metabolism to a ketogenic nutrient environment. J Biol Chem 2010; 285(32): 24447-56.
[http://dx.doi.org/10.1074/jbc.M110.100651] [PMID: 20529848]
[88]
Walklate J, Ujfalusi Z, Geeves MA. Myosin isoforms and the mechanochemical cross-bridge cycle. J Exp Biol 2016; 219(Pt 2): 168-74.
[http://dx.doi.org/10.1242/jeb.124594] [PMID: 26792327]
[89]
Balaban RS. The role of Ca(2+) signaling in the coordination of mitochondrial ATP production with cardiac work. Biochim Biophys Acta 2009; 1787(11): 1334-41.
[http://dx.doi.org/10.1016/j.bbabio.2009.05.011] [PMID: 19481532]
[90]
De Stefani D, Raffaello A, Teardo E, Szabò I, Rizzuto R. A forty-kilodalton protein of the inner membrane is the mitochondrial calcium uniporter. Nature 2011; 476(7360): 336-40.
[http://dx.doi.org/10.1038/nature10230] [PMID: 21685888]
[91]
Hajnóczky G, Robb-Gaspers LD, Seitz MB, Thomas AP. Decoding of cytosolic calcium oscillations in the mitochondria. Cell 1995; 82(3): 415-24.
[http://dx.doi.org/10.1016/0092-8674(95)90430-1] [PMID: 7634331]
[92]
Rizzuto R, Pinton P, Carrington W, et al. Close contacts with the endoplasmic reticulum as determinants of mitochondrial Ca2+ responses. Science 1998; 280(5370): 1763-6.
[http://dx.doi.org/10.1126/science.280.5370.1763] [PMID: 9624056]
[93]
Giorgi C, Marchi S, Pinton P. The machineries, regulation and cellular functions of mitochondrial calcium. Nat Rev Mol Cell Biol 2018; 19(11): 713-30.
[http://dx.doi.org/10.1038/s41580-018-0052-8] [PMID: 30143745]
[94]
Palty R, Silverman WF, Hershfinkel M, et al. NCLX is an essential component of mitochondrial Na+/Ca2+ exchange. Proc Natl Acad Sci USA 2010; 107(1): 436-41.
[http://dx.doi.org/10.1073/pnas.0908099107] [PMID: 20018762]
[95]
Brown DA, Perry JB, Allen ME, et al. Expert consensus document: Mitochondrial function as a therapeutic target in heart failure. Nat Rev Cardiol 2017; 14(4): 238-50.
[http://dx.doi.org/10.1038/nrcardio.2016.203] [PMID: 28004807]
[96]
Abel ED. Obesity stresses cardiac mitochondria even when you are young. J Am Coll Cardiol 2011; 57(5): 586-9.
[http://dx.doi.org/10.1016/j.jacc.2010.09.039] [PMID: 21272750]
[97]
Niemann B, Chen Y, Teschner M, Li L, Silber R-E, Rohrbach S. Obesity induces signs of premature cardiac aging in younger patients: The role of mitochondria. J Am Coll Cardiol 2011; 57(5): 577-85.
[http://dx.doi.org/10.1016/j.jacc.2010.09.040] [PMID: 21272749]
[98]
Stacchiotti A, Favero G, Giugno L, Golic I, Korac A, Rezzani R. Melatonin efficacy in obese leptin-deficient mice heart. Nutrients 2017; 9(12)E1323
[http://dx.doi.org/10.3390/nu9121323] [PMID: 29206172]
[99]
Gottlieb RA, Thomas A. Mitophagy and mitochondrial quality control mechanisms in the heart. Curr Pathobiol Rep 2017; 5(2): 161-9.
[http://dx.doi.org/10.1007/s40139-017-0133-y] [PMID: 29082112]
[100]
Zeng H, Vaka VR, He X, Booz GW, Chen J-X. High-fat diet induces cardiac remodelling and dysfunction: Assessment of the role played by SIRT3 loss. J Cell Mol Med 2015; 19(8): 1847-56.
[http://dx.doi.org/10.1111/jcmm.12556] [PMID: 25782072]
[101]
Kendrick AA, Choudhury M, Rahman SM, et al. Fatty liver is associated with reduced SIRT3 activity and mitochondrial protein hyperacetylation. Biochem J 2011; 433(3): 505-14.
[http://dx.doi.org/10.1042/BJ20100791] [PMID: 21044047]
[102]
de Moura Freitas C, do Nascimento LCP, Braz GRF, et al. Mitochondrial impairment following neonatal overfeeding: A comparison between normal and ischemic-reperfused hearts. J Cell Biochem 2018. In Press
[103]
Ferey JLA, Boudoures AL, Reid M, et al. A maternal high-fat, high-sucrose diet induces transgenerational cardiac mitochondrial dysfunction independently of maternal mitochondrial inheritance. Am J Physiol Heart Circ Physiol 2019; 316(5): H1202-10.
[http://dx.doi.org/10.1152/ajpheart.00013.2019] [PMID: 30901280]
[104]
López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell 2013; 153(6): 1194-217.
[http://dx.doi.org/10.1016/j.cell.2013.05.039] [PMID: 23746838]
[105]
Bratic A, Larsson NG. The role of mitochondria in aging. J Clin Invest 2013; 123(3): 951-7.
[http://dx.doi.org/10.1172/JCI64125] [PMID: 23454757]
[106]
Gonzalez-Freire M, De Cabo R, Bernier M, et al. Reconsidering the role of mitochondria in aging. J Gerontol Ser A Biol Sci Med Sci 2015; 70(11): 1334-42.
[107]
Lane RK, Hilsabeck T, Rea SL. The role of mitochondrial dysfunction in age-related diseases. Biochim Biophys Acta 2015; 1847(11): 1387-400.
[http://dx.doi.org/10.1016/j.bbabio.2015.05.021] [PMID: 26050974]
[108]
Payne BAI, Chinnery PF. Mitochondrial dysfunction in aging: Much progress but many unresolved questions. Biochim Biophys Acta 2015; 1847(11): 1347-53.
[http://dx.doi.org/10.1016/j.bbabio.2015.05.022] [PMID: 26050973]
[109]
Harman D. Aging: A theory based on free radical and radiation chemistry. J Gerontol 1956; 11(3): 298-300.
[http://dx.doi.org/10.1093/geronj/11.3.298] [PMID: 13332224]
[110]
Balaban RS, Nemoto S, Finkel T. Mitochondria, oxidants, and aging. Cell 2005; 120(4): 483-95.
[http://dx.doi.org/10.1016/j.cell.2005.02.001] [PMID: 15734681]
[111]
Parodi-Rullán RM, Chapa-Dubocq XR, Javadov S. Acetylation of mitochondrial proteins in the heart: The role of SIRT3. Front Physiol 2018; 9: 1094.
[http://dx.doi.org/10.3389/fphys.2018.01094] [PMID: 30131726]
[112]
Matsushima S, Sadoshima J. The role of sirtuins in cardiac disease. Am J Physiol Heart Circ Physiol 2015; 309(9): H1375-89.
[http://dx.doi.org/10.1152/ajpheart.00053.2015] [PMID: 26232232]
[113]
Sadoshima J. Sirt3 targets mPTP and prevents aging in the heart. Aging (Albany NY) 2011; 3(1): 12-3.
[http://dx.doi.org/10.18632/aging.100266] [PMID: 21248376]
[114]
He X, Zeng H, Chen J-X. Ablation of SIRT3 causes coronary microvascular dysfunction and impairs cardiac recovery post myocardial ischemia. Int J Cardiol 2016; 215: 349-57.
[http://dx.doi.org/10.1016/j.ijcard.2016.04.092] [PMID: 27128560]
[115]
Cosentino F, Francia P, Camici GG, Pelicci PG, Lüscher TF, Volpe M. Final common molecular pathways of aging and cardiovascular disease: Role of the p66Shc protein. Arterioscler Thromb Vasc Biol 2008; 28(4): 622-8.
[http://dx.doi.org/10.1161/ATVBAHA.107.156059] [PMID: 18162611]
[116]
Camici GG, Savarese G, Akhmedov A, Lüscher TF. Molecular mechanism of endothelial and vascular aging: Implications for cardiovascular disease. Eur Heart J 2015; 36(48): 3392-403.
[http://dx.doi.org/10.1093/eurheartj/ehv587] [PMID: 26543043]
[117]
Migliaccio E, Giorgio M, Mele S, et al. The p66shc adaptor protein controls oxidative stress response and life span in mammals. Nature 1999; 402(6759): 309-13.
[http://dx.doi.org/10.1038/46311] [PMID: 10580504]
[118]
Shi Y, Savarese G, Perrone-Filardi P, Lüscher TF, Camici GG. Enhanced age-dependent cerebrovascular dysfunction is mediated by adaptor protein p66Shc. Int J Cardiol 2014; 175(3): 446-50.
[http://dx.doi.org/10.1016/j.ijcard.2014.06.025] [PMID: 25012499]
[119]
Spescha RD, Glanzmann M, Simic B, et al. Adaptor protein p66(Shc) mediates hypertension-associated, cyclic stretch-dependent, endothelial damage. Hypertension 2014; 64(2): 347-53.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.113.02129] [PMID: 24842918]
[120]
Spescha RD, Shi Y, Wegener S, et al. Deletion of the ageing gene p66(Shc) reduces early stroke size following ischaemia/reperfusion brain injury. Eur Heart J 2013; 34(2): 96-103.
[http://dx.doi.org/10.1093/eurheartj/ehs331] [PMID: 23008506]
[121]
Lee W-H, Higuchi H, Ikeda S, et al. Mouse Tmem135 mutation reveals a mechanism involving mitochondrial dynamics that leads to age-dependent retinal pathologies. eLife 2016; 5e19264
[http://dx.doi.org/10.7554/eLife.19264] [PMID: 27863209]
[122]
Song M, Mihara K, Chen Y, Scorrano L, Dorn GW II. Mitochondrial fission and fusion factors reciprocally orchestrate mitophagic culling in mouse hearts and cultured fibroblasts. Cell Metab 2015; 21(2): 273-86.
[http://dx.doi.org/10.1016/j.cmet.2014.12.011] [PMID: 25600785]
[123]
Lewis SA, Takimoto T, Mehrvar S, et al. The effect of Tmem135 overexpression on the mouse heart. PLoS One 2018; 13(8)e0201986
[http://dx.doi.org/10.1371/journal.pone.0201986] [PMID: 30102730]
[124]
Corral-Debrinski M, Shoffner JM, Lott MT, Wallace DC. Association of mitochondrial DNA damage with aging and coronary atherosclerotic heart disease. Mutat Res 1992; 275(3-6): 169-80.
[http://dx.doi.org/10.1016/0921-8734(92)90021-G] [PMID: 1383759]
[125]
Li YY, Hengstenberg C, Maisch B. Whole mitochondrial genome amplification reveals basal level multiple deletions in mtDNA of patients with dilated cardiomyopathy. Biochem Biophys Res Commun 1995; 210(1): 211-8.
[http://dx.doi.org/10.1006/bbrc.1995.1648] [PMID: 7741744]
[126]
Dai D-F, Chen T, Wanagat J, et al. Age-dependent cardiomyopathy in mitochondrial mutator mice is attenuated by overexpression of catalase targeted to mitochondria. Aging Cell 2010; 9(4): 536-44.
[http://dx.doi.org/10.1111/j.1474-9726.2010.00581.x] [PMID: 20456298]
[127]
Matthews PM, Hopkin J, Brown RM, Stephenson JB, Hilton-Jones D, Brown GK. Comparison of the relative levels of the 3243 (A-->G) mtDNA mutation in heteroplasmic adult and fetal tissues. J Med Genet 1994; 31(1): 41-4.
[http://dx.doi.org/10.1136/jmg.31.1.41] [PMID: 8151636]
[128]
Tranah GJ, Katzman SM, Lauterjung K, et al. Mitochondrial DNA m.3243A > G heteroplasmy affects multiple aging phenotypes and risk of mortality. Sci Rep 2018; 8(1): 11887.
[http://dx.doi.org/10.1038/s41598-018-30255-6] [PMID: 30089816]
[129]
Bugger H, Abel ED. Mitochondria in the diabetic heart. Cardiovasc Res 2010; 88(2): 229-40.
[http://dx.doi.org/10.1093/cvr/cvq239] [PMID: 20639213]
[130]
Duncan JG. Mitochondrial dysfunction in diabetic cardiomyopathy. Biochim Biophys Acta 2011; 1813(7): 1351-9.
[http://dx.doi.org/10.1016/j.bbamcr.2011.01.014] [PMID: 21256163]
[131]
Mazumder PK, O’Neill BT, Roberts MW, et al. Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts. Diabetes 2004; 53(9): 2366-74.
[http://dx.doi.org/10.2337/diabetes.53.9.2366] [PMID: 15331547]
[132]
Buchanan J, Mazumder PK, Hu P, et al. Reduced cardiac efficiency and altered substrate metabolism precedes the onset of hyperglycemia and contractile dysfunction in two mouse models of insulin resistance and obesity. Endocrinology 2005; 146(12): 5341-9.
[http://dx.doi.org/10.1210/en.2005-0938] [PMID: 16141388]
[133]
Rasool S, Geetha T, Broderick TL, Babu JR. High fat with high sucrose diet leads to obesity and induces myodegeneration. Front Physiol 2018; 9: 1054.
[http://dx.doi.org/10.3389/fphys.2018.01054] [PMID: 30258366]
[134]
Vadvalkar SS, Matsuzaki S, Eyster CA, et al. Decreased mitochondrial pyruvate transport activity in the diabetic heart: Role of mitochondrial pyruvate carrier 2 (MPC2) acetylation. J Biol Chem 2017; 292(11): 4423-33.
[http://dx.doi.org/10.1074/jbc.M116.753509] [PMID: 28154187]
[135]
Koentges C, Pfeil K, Schnick T, et al. SIRT3 deficiency impairs mitochondrial and contractile function in the heart. Basic Res Cardiol 2015; 110(4): 36.
[http://dx.doi.org/10.1007/s00395-015-0493-6] [PMID: 25962702]
[136]
Gui J, Potthast A, Rohrbach A, Borns K, Das AM, von Versen-Höynck F. Gestational diabetes induces alterations of sirtuins in fetal endothelial cells. Pediatr Res 2016; 79(5): 788-98.
[http://dx.doi.org/10.1038/pr.2015.269] [PMID: 26717002]
[137]
Camici GG, Schiavoni M, Francia P, et al. Genetic deletion of p66(Shc) adaptor protein prevents hyperglycemia-induced endothelial dysfunction and oxidative stress. Proc Natl Acad Sci USA 2007; 104(12): 5217-22.
[http://dx.doi.org/10.1073/pnas.0609656104] [PMID: 17360381]
[138]
Pagnin E, Fadini G, de Toni R, Tiengo A, Calò L, Avogaro A. Diabetes induces p66shc gene expression in human peripheral blood mononuclear cells: Relationship to oxidative stress. J Clin Endocrinol Metab 2005; 90(2): 1130-6.
[http://dx.doi.org/10.1210/jc.2004-1283] [PMID: 15562031]
[139]
Li W, Yao M, Wang R, et al. Profile of cardiac lipid metabolism in STZ-induced diabetic mice. Lipids Health Dis 2018; 17(1): 231.
[http://dx.doi.org/10.1186/s12944-018-0872-8] [PMID: 30301464]
[140]
Edwards KS, Ashraf S, Lomax TM, et al. Uncoupling protein 3 deficiency impairs myocardial fatty acid oxidation and contractile recovery following ischemia/reperfusion. Basic Res Cardiol 2018; 113(6): 47.
[http://dx.doi.org/10.1007/s00395-018-0707-9] [PMID: 30374710]
[141]
Riojas-Hernández A, Bernal-Ramírez J, Rodríguez-Mier D, et al. Enhanced oxidative stress sensitizes the mitochondrial permeability transition pore to opening in heart from Zucker Fa/fa rats with type 2 diabetes. Life Sci 2015; 141: 32-43.
[http://dx.doi.org/10.1016/j.lfs.2015.09.018] [PMID: 26407476]
[142]
Sloan RC, Moukdar F, Frasier CR, et al. Mitochondrial permeability transition in the diabetic heart: Contributions of thiol redox state and mitochondrial calcium to augmented reperfusion injury. J Mol Cell Cardiol 2012; 52(5): 1009-18.
[http://dx.doi.org/10.1016/j.yjmcc.2012.02.009] [PMID: 22406429]
[143]
Lumini-Oliveira J, Magalhães J, Pereira CV, Moreira AC, Oliveira PJ, Ascensão A. Endurance training reverts heart mitochondrial dysfunction, permeability transition and apoptotic signaling in long-term severe hyperglycemia. Mitochondrion 2011; 11(1): 54-63.
[http://dx.doi.org/10.1016/j.mito.2010.07.005] [PMID: 20654738]
[144]
Bertero E, Maack C. Calcium signaling and reactive oxygen species in mitochondria. Circ Res 2018; 122(10): 1460-78.
[http://dx.doi.org/10.1161/CIRCRESAHA.118.310082] [PMID: 29748369]
[145]
Epstein PN, Overbeek PA, Means AR. Calmodulin-induced early-onset diabetes in transgenic mice. Cell 1989; 58(6): 1067-73.
[http://dx.doi.org/10.1016/0092-8674(89)90505-9] [PMID: 2673540]
[146]
Epstein PN, Ribar TJ, Decker GL, Yaney G, Means AR. Elevated beta-cell calmodulin produces a unique insulin secretory defect in transgenic mice. Endocrinology 1992; 130(3): 1387-93.
[PMID: 1371447]
[147]
Yu W, Niwa T, Miura Y, et al. Calmodulin overexpression causes Ca(2+)-dependent apoptosis of pancreatic beta cells, which can be prevented by inhibition of nitric oxide synthase. Lab Invest 2002; 82(9): 1229-39.
[http://dx.doi.org/10.1097/01.LAB.0000027921.01548.C5] [PMID: 12218084]
[148]
Koves TR, Ussher JR, Noland RC, et al. Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance. Cell Metab 2008; 7(1): 45-56.
[http://dx.doi.org/10.1016/j.cmet.2007.10.013] [PMID: 18177724]
[149]
Zhang L, Keung W, Samokhvalov V, Wang W, Lopaschuk GD. Role of fatty acid uptake and fatty acid β-oxidation in mediating insulin resistance in heart and skeletal muscle. Biochim Biophys Acta 2010; 1801(1): 1-22.
[http://dx.doi.org/10.1016/j.bbalip.2009.09.014] [PMID: 19782765]
[150]
Bugger H, Boudina S, Hu XX, et al. Type 1 diabetic akita mouse hearts are insulin sensitive but manifest structurally abnormal mitochondria that remain coupled despite increased uncoupling protein 3. Diabetes 2008; 57(11): 2924-32.
[http://dx.doi.org/10.2337/db08-0079] [PMID: 18678617]
[151]
Bugger H, Chen D, Riehle C, et al. Tissue-specific remodeling of the mitochondrial proteome in type 1 diabetic akita mice. Diabetes 2009; 58(9): 1986-97.
[http://dx.doi.org/10.2337/db09-0259] [PMID: 19542201]
[152]
Yoshioka M, Kayo T, Ikeda T, Koizuni A. A novel locus, mody4, distal to D7Mit189 on chromosome 7 determines early-onset NIDDM in nonobese C57BL/6 (Akita) mutant mice. Diabetes 1997; 46(5): 887-94.
[153]
Wang J, Takeuchi T, Tanaka S, et al. A mutation in the insulin 2 gene induces diabetes with severe pancreatic β-cell dysfunction in the Mody mouse. J Clin Invest 1999; 103(1): 27-37.
[http://dx.doi.org/10.1172/JCI4431] [PMID: 9884331]
[154]
Basu R, Oudit GY, Wang X, et al. Type 1 diabetic cardiomyopathy in the Akita (Ins2WT/C96Y) mouse model is characterized by lipotoxicity and diastolic dysfunction with preserved systolic function. Am J Physiol Heart Circ Physiol 2009; 297(6): H2096-108.
[http://dx.doi.org/10.1152/ajpheart.00452.2009] [PMID: 19801494]
[155]
Pulinilkunnil T, Kienesberger PC, Nagendran J, et al. Myocardial adipose triglyceride lipase overexpression protects diabetic mice from the development of lipotoxic cardiomyopathy. Diabetes 2013; 62(5): 1464-77.
[http://dx.doi.org/10.2337/db12-0927] [PMID: 23349479]
[156]
Schaffner F, Thaler H. Nonalcoholic fatty liver disease. Prog Liver Dis 1986; 8: 283-98.
[PMID: 3086934]
[157]
Smith BW, Adams LA. Non-alcoholic fatty liver disease. Crit Rev Clin Lab Sci 1997; 48(3): 97-113.
[http://dx.doi.org/10.3109/10408363.2011.596521]
[158]
Fotbolcu H, Zorlu E. Nonalcoholic fatty liver disease as a multi-systemic disease. World J Gastroenterol 2016; 22(16): 4079-90.
[http://dx.doi.org/10.3748/wjg.v22.i16.4079] [PMID: 27122660]
[159]
Targher G, Day CP, Bonora E. Risk of cardiovascular disease in patients with nonalcoholic fatty liver disease. N Engl J Med 2010; 363(14): 1341-50.
[http://dx.doi.org/10.1056/NEJMra0912063] [PMID: 20879883]
[160]
Adams LA, Anstee QM, Tilg H, Targher G. Non-alcoholic fatty liver disease and its relationship with cardiovascular disease and other extrahepatic diseases. Gut 2017; 66(6): 1138-53.
[http://dx.doi.org/10.1136/gutjnl-2017-313884] [PMID: 28314735]
[161]
Targher G, Byrne CD, Lonardo A, Zoppini G, Barbui C. Non-alcoholic fatty liver disease and risk of incident cardiovascular disease: A meta-analysis. J Hepatol 2016; 65(3): 589-600.
[http://dx.doi.org/10.1016/j.jhep.2016.05.013] [PMID: 27212244]
[162]
Nakajima T, Fujioka S, Tokunaga K, Matsuzawa Y, Tarui S. Correlation of intraabdominal fat accumulation and left ventricular performance in obesity. Am J Cardiol 1989; 64(5): 369-73.
[http://dx.doi.org/10.1016/0002-9149(89)90537-7] [PMID: 2756882]
[163]
Degli Esposti D, Hamelin J, Bosselut N, et al. Mitochondrial roles and cytoprotection in chronic liver injury. Biochem Res Int 2012; 2012387626
[http://dx.doi.org/10.1155/2012/387626] [PMID: 22745910]
[164]
Simões ICM, Fontes A, Pinton P, Zischka H, Wieckowski MR. Mitochondria in non-alcoholic fatty liver disease. Int J Biochem Cell Biol 2018; 95: 93-9.
[http://dx.doi.org/10.1016/j.biocel.2017.12.019] [PMID: 29288054]
[165]
Grattagliano I, Montezinho LP, Oliveira PJ, et al. Targeting mitochondria to oppose the progression of nonalcoholic fatty liver disease. Biochem Pharmacol 2019; 160(160): 34-45.
[http://dx.doi.org/10.1016/j.bcp.2018.11.020] [PMID: 30508523]
[166]
Begriche K, Igoudjil A, Pessayre D, Fromenty B. Mitochondrial dysfunction in NASH: Causes, consequences and possible means to prevent it. Mitochondrion 2006; 6(1): 1-28.
[http://dx.doi.org/10.1016/j.mito.2005.10.004] [PMID: 16406828]
[167]
Satapati S, Kucejova B, Duarte JAG, et al. Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver. J Clin Invest 2015; 125(12): 4447-62.
[http://dx.doi.org/10.1172/JCI82204] [PMID: 26571396]
[168]
Chess DJ, Stanley WC. Role of diet and fuel overabundance in the development and progression of heart failure. Cardiovasc Res 2008; 79(2): 269-78.
[http://dx.doi.org/10.1093/cvr/cvn074] [PMID: 18343896]
[169]
Kim BJ, Kim HS, Kang JG, Kim BS, Kang JH. Association of epicardial fat volume and nonalcoholic fatty liver disease with metabolic syndrome: From the CAESAR study. J Clin Lipidol 2016; 10(6): 1423-30.e1.
[http://dx.doi.org/10.1016/j.jacl.2016.09.007] [PMID: 27919360]
[170]
Meng X, Wang W, Zhang K, et al. Epicardial adipose tissue volume is associated with non-alcoholic fatty liver disease and cardiovascular risk factors in the general population. Ther Clin Risk Manag 2018; 14: 1499-506.
[http://dx.doi.org/10.2147/TCRM.S168345] [PMID: 30197519]
[171]
Nie H, Pan Y, Zhou Y. Exosomal microRNA-194 causes cardiac injury and mitochondrial dysfunction in obese mice. Biochem Biophys Res Commun 2018; 503(4): 3174-9.
[http://dx.doi.org/10.1016/j.bbrc.2018.08.113] [PMID: 30170731]
[172]
Chen D, Li X, Zhang L, Zhu M, Gao L. A high-fat diet impairs mitochondrial biogenesis, mitochondrial dynamics, and the respiratory chain complex in rat myocardial tissues. J Cell Biochem 2018; 119(11): 9602.
[http://dx.doi.org/10.1002/jcb.27068] [PMID: 30171706]
[173]
Marín-Royo G, Ortega-Hernández A, Martínez-Martínez E, et al. The impact of cardiac lipotoxicity on cardiac function and mirnas signature in obese and non-obese rats with myocardial infarction. Sci Rep 2019; 9(1): 444.
[http://dx.doi.org/10.1038/s41598-018-36914-y] [PMID: 30679580]
[174]
Peterson LR, Xanthakis V, Duncan MS, et al. Ceramide remodeling and risk of cardiovascular events and mortality. J Am Heart Assoc 2018; 7(10)e007931
[http://dx.doi.org/10.1161/JAHA.117.007931] [PMID: 29728014]
[175]
Murray AJ, Cole MA, Lygate CA, et al. Increased mitochondrial uncoupling proteins, respiratory uncoupling and decreased efficiency in the chronically infarcted rat heart. J Mol Cell Cardiol 2008; 44(4): 694-700.
[http://dx.doi.org/10.1016/j.yjmcc.2008.01.008] [PMID: 18328500]
[176]
Laskowski KR, Russell RR III. Uncoupling proteins in heart failure. Curr Heart Fail Rep 2008; 5(2): 75-9.
[http://dx.doi.org/10.1007/s11897-008-0013-1] [PMID: 18765077]
[177]
Jin X, Xiang Z, Chen YP, Ma KF, Ye YF, Li YM. Uncoupling protein and nonalcoholic fatty liver disease. Chin Med J (Engl) 2013; 126(16): 3151-5.
[PMID: 23981628]
[178]
Baffy G, Zhang C-Y, Glickman JN, Lowell BB. Obesity-related fatty liver is unchanged in mice deficient for mitochondrial uncoupling protein 2. Hepatology 2002; 35(4): 753-61.
[http://dx.doi.org/10.1053/jhep.2002.32028] [PMID: 11915020]
[179]
Al-Khader AA. The cardio-renal syndrome. Nephron 1988; 48(1): 86.
[http://dx.doi.org/10.1159/000184880] [PMID: 3340265]
[180]
Ronco C, McCullough P, Anker SD, et al. Acute Dialysis Quality Initiative (ADQI) consensus group. Cardio-renal syndromes: Report from the consensus conference of the acute dialysis quality initiative. Eur Heart J 2010; 31(6): 703-11.
[http://dx.doi.org/10.1093/eurheartj/ehp507] [PMID: 20037146]
[181]
McCullough PA, Ahmad A. Cardiorenal syndromes. World J Cardiol 2011; 3(1): 1-9.
[http://dx.doi.org/10.4330/wjc.v3.i1.1] [PMID: 21286212]
[182]
Di Lullo L, Bellasi A, Barbera V, et al. Pathophysiology of the cardio-renal syndromes types 1-5: An uptodate. Indian Heart J 2017; 69(2): 255-65.
[http://dx.doi.org/10.1016/j.ihj.2017.01.005] [PMID: 28460776]
[183]
Bigelman E, Cohen L, Aharon-Hananel G, et al. Pathological presentation of cardiac mitochondria in a rat model for chronic kidney disease. PLoS One 2018; 13(6)e0198196
[http://dx.doi.org/10.1371/journal.pone.0198196] [PMID: 29889834]
[184]
Eirin A, Ebrahimi B, Kwon SH, et al. Restoration of mitochondrial cardiolipin attenuates cardiac damage in swine renovascular hypertension. J Am Heart Assoc 2016; 5(6)e003118
[http://dx.doi.org/10.1161/JAHA.115.003118] [PMID: 27247333]
[185]
Dudek J, Hartmann M, Rehling P. The role of mitochondrial cardiolipin in heart function and its implication in cardiac disease. Biochim Biophys Acta Mol Basis Dis 2019; 1865(4): 810-21.
[http://dx.doi.org/10.1016/j.bbadis.2018.08.025] [PMID: 30837070]
[186]
Sumida M, Doi K, Ogasawara E, et al. Regulation of mitochondrial dynamics by dynamin-related protein-1 in acute cardiorenal syndrome. J Am Soc Nephrol 2015; 26(10): 2378-87.
[http://dx.doi.org/10.1681/ASN.2014080750] [PMID: 25644112]
[187]
Moore SC, Patel AV, Matthews CE, et al. Leisure time physical activity of moderate to vigorous intensity and mortality: A large pooled cohort analysis. PLoS Med 2012; 9(11)e1001335
[http://dx.doi.org/10.1371/journal.pmed.1001335] [PMID: 23139642]
[188]
Bhella PS, Hastings JL, Fujimoto N, et al. Impact of lifelong exercise “dose” on left ventricular compliance and distensibility. J Am Coll Cardiol 2014; 64(12): 1257-66.
[http://dx.doi.org/10.1016/j.jacc.2014.03.062] [PMID: 25236519]
[189]
Carson V, Ridgers ND, Howard BJ, et al. Light-intensity physical activity and cardiometabolic biomarkers in US adolescents. PLoS One 2013; 8(8)e71417
[http://dx.doi.org/10.1371/journal.pone.0071417] [PMID: 23951157]
[190]
WHO. Global recommendations on physical activity for health. 2010; p. 58.
[191]
WHO. WHO. Guidelines on physical activity, sedentary behaviour and sleep for children under 5 years of age. 2019; p. 33.
[192]
Lee D-C, Pate RR, Lavie CJ, Sui X, Church TS, Blair SN. Leisure-time running reduces all-cause and cardiovascular mortality risk. J Am Coll Cardiol 2014; 64(5): 472-81.
[http://dx.doi.org/10.1016/j.jacc.2014.04.058] [PMID: 25082581]
[193]
Kohl HW III, Craig CL, Lambert EV, et al. The pandemic of physical inactivity: Global action for public health. Lancet 2012; 380(9838): 294-305.
[http://dx.doi.org/10.1016/S0140-6736(12)60898-8] [PMID: 22818941]
[194]
WHO. Global health risks: mortality and burden of disease attributable to selected major risks. 2009; p. 62.
[195]
Quindry JC, Hamilton KL. Exercise and cardiac preconditioning against ischemia reperfusion injury. Curr Cardiol Rev 2013; 9(3): 220-9.
[http://dx.doi.org/10.2174/1573403X113099990033] [PMID: 23909636]
[196]
Downey JM. Free radicals and their involvement during long-term myocardial ischemia and reperfusion. Annu Rev Physiol 1990; 52: 487-504.
[http://dx.doi.org/10.1146/annurev.ph.52.030190.002415] [PMID: 2184765]
[197]
Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med 2007; 357(11): 1121-35.
[http://dx.doi.org/10.1056/NEJMra071667] [PMID: 17855673]
[198]
Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: A delay of lethal cell injury in ischemic myocardium. Circulation 1986; 74(5): 1124-36.
[http://dx.doi.org/10.1161/01.CIR.74.5.1124] [PMID: 3769170]
[199]
Bowles DK, Farrar RP, Starnes JW. Exercise training improves cardiac function after ischemia in the isolated, working rat heart. Am J Physiol 1992; 263(3Pt.2): H804-9.
[PMID: 1415606]
[200]
Hoshida S, Yamashita N, Otsu K, Hori M. Repeated physiologic stresses provide persistent cardioprotection against ischemia-reperfusion injury in rats. J Am Coll Cardiol 2002; 40(4): 826-31.
[http://dx.doi.org/10.1016/S0735-1097(02)02001-6] [PMID: 12204517]
[201]
Libonati JR, Gaughan JP, Hefner CA, Gow A, Paolone AM, Houser SR. Reduced ischemia and reperfusion injury following exercise training. Med Sci Sports Exerc 1997; 29(4): 509-16.
[http://dx.doi.org/10.1097/00005768-199704000-00013] [PMID: 9107634]
[202]
Quindry JC, Schreiber L, Hosick P, Wrieden J, Irwin JM, Hoyt E. Mitochondrial KATP channel inhibition blunts arrhythmia protection in ischemic exercised hearts. Am J Physiol Heart Circ Physiol 2010; 299(1): H175-83.
[http://dx.doi.org/10.1152/ajpheart.01211.2009] [PMID: 20435852]
[203]
DeVan AE, Umpierre D, Lin H-F, et al. Habitual resistance exercise and endothelial ischemia-reperfusion injury in young adults. Atherosclerosis 2011; 219(1): 191-3.
[http://dx.doi.org/10.1016/j.atherosclerosis.2011.07.099] [PMID: 21840524]
[204]
Maessen MFH, van Mil ACCM, Straathof Y, et al. Impact of lifelong exercise training on endothelial ischemia-reperfusion and ischemic preconditioning in humans. Am J Physiol Regul Integr Comp Physiol 2017; 312(5): R828-34.
[http://dx.doi.org/10.1152/ajpregu.00466.2016] [PMID: 28298332]
[205]
Campos JC, Queliconi BB, Dourado PMM, et al. Exercise training restores cardiac protein quality control in heart failure. PLoS One 2012; 7(12)e52764
[http://dx.doi.org/10.1371/journal.pone.0052764] [PMID: 23300764]
[206]
Gibb AA, Epstein PN, Uchida S, et al. Exercise-induced changes in glucose metabolism promote physiological cardiac growth. Circulation 2017; 136(22): 2144-57.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.117.028274] [PMID: 28860122]
[207]
Kavazis AN, Alvarez S, Talbert E, Lee Y, Powers SK. Exercise training induces a cardioprotective phenotype and alterations in cardiac subsarcolemmal and intermyofibrillar mitochondrial proteins. Am J Physiol Heart Circ Physiol 2009; 297(1): H144-52.
[http://dx.doi.org/10.1152/ajpheart.01278.2008] [PMID: 19429812]
[208]
French JP, Hamilton KL, Quindry JC, Lee Y, Upchurch PA, Powers SK. Exercise-induced protection against myocardial apoptosis and necrosis: MnSOD, calcium-handling proteins, and calpain. FASEB J 2008; 22(8): 2862-71.
[http://dx.doi.org/10.1096/fj.07-102541] [PMID: 18417547]
[209]
Quindry J, French J, Hamilton K, Lee Y, Mehta JL, Powers S. Exercise training provides cardioprotection against ischemia-reperfusion induced apoptosis in young and old animals. Exp Gerontol 2005; 40(5): 416-25.
[http://dx.doi.org/10.1016/j.exger.2005.03.010] [PMID: 15919594]
[210]
da Silva MF, Natali AJ, da Silva E, et al. Attenuation of Ca2+ homeostasis, oxidative stress, and mitochondrial dysfunctions in diabetic rat heart: Insulin therapy or aerobic exercise? J Appl Physiol (Bethesda, Md 1985) 2015; 15; 119(2): 148-56.
[211]
Ascensão A, Lumini-Oliveira J, Machado NG, et al. Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats. Clin Sci (London, Engl 1979) 2011; 120(1): 37-49.
[212]
Powers SK, Sollanek KJ, Wiggs MP, Demirel HA, Smuder AJ. Exercise-induced improvements in myocardial antioxidant capacity: The antioxidant players and cardioprotection. Free Radic Res 2014; 48(1): 43-51.
[http://dx.doi.org/10.3109/10715762.2013.825371] [PMID: 23915097]
[213]
Hamilton KL, Quindry JC, French JP, et al. MnSOD antisense treatment and exercise-induced protection against arrhythmias. Free Radic Biol Med 2004; 37(9): 1360-8.
[http://dx.doi.org/10.1016/j.freeradbiomed.2004.07.025] [PMID: 15454275]
[214]
Ascensão A, Magalhães J, Soares JMC, et al. Moderate endurance training prevents doxorubicin-induced in vivo mitochondriopathy and reduces the development of cardiac apoptosis. Am J Physiol Heart Circ Physiol 2005; 289(2): H722-31.
[http://dx.doi.org/10.1152/ajpheart.01249.2004] [PMID: 15792986]
[215]
Martin JL, Mestril R, Hilal-Dandan R, Brunton LL, Dillmann WH. Small heat shock proteins and protection against ischemic injury in cardiac myocytes. Circulation 1997; 96(12): 4343-8.
[http://dx.doi.org/10.1161/01.CIR.96.12.4343] [PMID: 9416902]
[216]
Rinaldi B, Corbi G, Boccuti S, et al. Exercise training affects age-induced changes in SOD and heat shock protein expression in rat heart. Exp Gerontol 2006; 41(8): 764-70.
[http://dx.doi.org/10.1016/j.exger.2006.05.008] [PMID: 16822632]
[217]
Chen K, Pittman RN, Popel AS. Nitric oxide in the vasculature: Where does it come from and where does it go? A quantitative perspective. Antioxid Redox Signal 2008; 10(7): 1185-98.
[http://dx.doi.org/10.1089/ars.2007.1959] [PMID: 18331202]
[218]
Hambrecht R, Adams V, Erbs S, et al. Regular physical activity improves endothelial function in patients with coronary artery disease by increasing phosphorylation of endothelial nitric oxide synthase. Circulation 2003; 107(25): 3152-8.
[http://dx.doi.org/10.1161/01.CIR.0000074229.93804.5C] [PMID: 12810615]
[219]
Borniquel S, Valle I, Cadenas S, Lamas S, Monsalve M. Nitric oxide regulates mitochondrial oxidative stress protection via the transcriptional coactivator PGC-1alpha. FASEB J 2006; 20(11): 1889-91.
[http://dx.doi.org/10.1096/fj.05-5189fje] [PMID: 16891621]
[220]
Nisoli E, Falcone S, Tonello C, et al. Mitochondrial biogenesis by NO yields functionally active mitochondria in mammals. Proc Natl Acad Sci USA 2004; 101(47): 16507-12.
[http://dx.doi.org/10.1073/pnas.0405432101] [PMID: 15545607]
[221]
Subbotina E, Sierra A, Zhu Z, et al. Musclin is an activity-stimulated myokine that enhances physical endurance. Proc Natl Acad Sci USA 2015; 112(52): 16042-7.
[http://dx.doi.org/10.1073/pnas.1514250112] [PMID: 26668395]
[222]
Willich SN, Lewis M, Löwel H, Arntz HR, Schubert F, Schröder R. Physical exertion as a trigger of acute myocardial infarction. N Engl J Med 1993; 329(23): 1684-90.
[http://dx.doi.org/10.1056/NEJM199312023292302] [PMID: 8232457]
[223]
Kavazis AN. Exercise preconditioning of the myocardium. Sports Med 2009; 39(11): 923-35.
[http://dx.doi.org/10.2165/11317870-000000000-00000] [PMID: 19827860]
[224]
Siasos G, Tsigkou V, Kosmopoulos M, et al. Mitochondria and cardiovascular diseases-from pathophysiology to treatment. Ann Transl Med 2018; 6(12): 256.
[http://dx.doi.org/10.21037/atm.2018.06.21] [PMID: 30069458]
[225]
Bayeva M, Gheorghiade M, Ardehali H. Mitochondria as a therapeutic target in heart failure. J Am Coll Cardiol 2013; 61(6): 599-610.
[http://dx.doi.org/10.1016/j.jacc.2012.08.1021] [PMID: 23219298]
[226]
Papageorgiou N, Tousoulis D, Katsargyris A, et al. Antioxidant treatment and endothelial dysfunction: Is it time for flavonoids? Recent Pat Cardiovasc Drug Discov 2013; 8(2): 81-92.
[http://dx.doi.org/10.2174/15748901113089990018] [PMID: 23952809]
[227]
Papageorgiou N, Tousoulis D, Androulakis E, et al. Lifestyle factors and endothelial function. Curr Vasc Pharmacol 2012; 10(1): 94-106.
[http://dx.doi.org/10.2174/157016112798829788] [PMID: 22112355]
[228]
Mercer JR. Mitochondrial bioenergetics and therapeutic intervention in cardiovascular disease. Pharmacol Ther 2014; 141(1): 13-20.
[http://dx.doi.org/10.1016/j.pharmthera.2013.07.011] [PMID: 23911986]
[229]
Bozaykut P, Karademir B, Yazgan B, et al. Effects of vitamin E on peroxisome proliferator-activated receptor γ and nuclear factor-erythroid 2-related factor 2 in hypercholesterolemia-induced atherosclerosis. Free Radic Biol Med 2014; 70: 174-81.
[http://dx.doi.org/10.1016/j.freeradbiomed.2014.02.017] [PMID: 24583459]
[230]
Garrido-Maraver J, Cordero MD, Oropesa-Avila M, et al. Clinical applications of coenzyme Q10. Front Biosci(Landmark Ed) 2014; 19: 619-33.
[http://dx.doi.org/10.2741/4231]
[231]
Graham D, Huynh NN, Hamilton CA, et al. Mitochondria-targeted antioxidant MitoQ10 improves endothelial function and attenuates cardiac hypertrophy. Hypertens (Dallas, Tex 1979) 1979; 54(2): 322-8.
[232]
Littarru GP, Langsjoen P. Coenzyme Q10 and statins: Biochemical and clinical implications. Mitochondrion 2007; 7(Suppl.): S168-74.
[http://dx.doi.org/10.1016/j.mito.2007.03.002] [PMID: 17482884]
[233]
Pepe S, Marasco SF, Haas SJ, Sheeran FL, Krum H, Rosenfeldt FL. Coenzyme Q10 in cardiovascular disease. Mitochondrion 2007; 7(Suppl.): S154-67.
[http://dx.doi.org/10.1016/j.mito.2007.02.005] [PMID: 17485243]
[234]
Smith RA, Porteous CM, Coulter CV, Murphy MP. Selective targeting of an antioxidant to mitochondria. Eur J Biochem 1999; 263(3): 709-16.
[http://dx.doi.org/10.1046/j.1432-1327.1999.00543.x] [PMID: 10469134]
[235]
Adlam VJ, Harrison JC, Porteous CM, et al. Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury. FASEB J 2005; 19(9): 1088-95.
[http://dx.doi.org/10.1096/fj.05-3718com] [PMID: 15985532]
[236]
McLachlan J, Beattie E, Murphy MP, et al. Combined therapeutic benefit of mitochondria-targeted antioxidant, MitoQ10, and angiotensin receptor blocker, losartan, on cardiovascular function. J Hypertens 2014; 32(3): 555-64.
[http://dx.doi.org/10.1097/HJH.0000000000000054] [PMID: 24309493]
[237]
Reily C, Mitchell T, Chacko BK, Benavides G, Murphy MP, Darley-Usmar V. Mitochondrially targeted compounds and their impact on cellular bioenergetics. Redox Biol 2013; 1(1): 86-93.
[http://dx.doi.org/10.1016/j.redox.2012.11.009] [PMID: 23667828]
[238]
Cochemé HM, Quin C, McQuaker SJ, et al. Measurement of H2O2 within living Drosophila during aging using a ratiometric mass spectrometry probe targeted to the mitochondrial matrix. Cell Metab 2011; 13(3): 340-50.
[http://dx.doi.org/10.1016/j.cmet.2011.02.003] [PMID: 21356523]
[239]
Robinson KM, Janes MS, Pehar M, et al. Selective fluorescent imaging of superoxide in vivo using ethidium-based probes. Proc Natl Acad Sci USA 2006; 103(41): 15038-43.
[http://dx.doi.org/10.1073/pnas.0601945103] [PMID: 17015830]
[240]
Prime TA, Forkink M, Logan A, et al. A ratiometric fluorescent probe for assessing mitochondrial phospholipid peroxidation within living cells. Free Radic Biol Med 2012; 53(3): 544-53.
[http://dx.doi.org/10.1016/j.freeradbiomed.2012.05.033] [PMID: 22659314]
[241]
Prime TA, Blaikie FH, Evans C, et al. A mitochondria-targeted S-nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury. Proc Natl Acad Sci USA 2009; 106(26): 10764-9.
[http://dx.doi.org/10.1073/pnas.0903250106] [PMID: 19528654]
[242]
Pucheu S, Boucher F, Sulpice T, et al. EUK-8 a synthetic catalytic scavenger of reactive oxygen species protects isolated iron-overloaded rat heart from functional and structural damage induced by ischemia/reperfusion. Cardiovasc Drugs Ther 1996; 10(3): 331-9.
[http://dx.doi.org/10.1007/BF02627957] [PMID: 8877076]
[243]
Cheng J, Kamiya K, Kodama I. Carvedilol: Molecular and cellular basis for its multifaceted therapeutic potential. Cardiovasc Drug Rev 2001; 19(2): 152-71.
[http://dx.doi.org/10.1111/j.1527-3466.2001.tb00061.x] [PMID: 11484068]
[244]
Pereira GC, Silva AM, Diogo CV, Carvalho FS, Monteiro P, Oliveira PJ. Drug-induced cardiac mitochondrial toxicity and protection: From doxorubicin to carvedilol. Curr Pharm Des 2011; 17(20): 2113-29.
[http://dx.doi.org/10.2174/138161211796904812] [PMID: 21718248]
[245]
Oliveira PJ, Esteves T, Rolo AP, Palmeira CM, Moreno AJM. Carvedilol inhibits the mitochondrial permeability transition by an antioxidant mechanism. Cardiovasc Toxicol 2004; 4(1): 11-20.
[http://dx.doi.org/10.1385/CT:4:1:11] [PMID: 15034201]
[246]
Oliveira PJ, Rolo AP, Palmeira CM, Moreno AJ. Carvedilol reduces mitochondrial damage induced by hypoxanthine/xanthine oxidase: Relevance to hypoxia/reoxygenation injury. Cardiovasc Toxicol 2001; 1(3): 205-13.
[http://dx.doi.org/10.1385/CT:1:3:205] [PMID: 12213973]
[247]
Oliveira PJ, Coxito PM, Rolo AP, Santos DL, Palmeira CM, Moreno AJ. Inhibitory effect of carvedilol in the high-conductance state of the mitochondrial permeability transition pore. Eur J Pharmacol 2001; 412(3): 231-7.
[http://dx.doi.org/10.1016/S0014-2999(01)00745-2] [PMID: 11166286]
[248]
Oliveira PJ, Bjork JA, Santos MS, et al. Carvedilol-mediated antioxidant protection against doxorubicin-induced cardiac mitochondrial toxicity. Toxicol Appl Pharmacol 2004; 200(2): 159-68.
[http://dx.doi.org/10.1016/j.taap.2004.04.005] [PMID: 15476868]
[249]
Sgobbo P, Pacelli C, Grattagliano I, Villani G, Cocco T. Carvedilol inhibits mitochondrial complex I and induces resistance to H2O2 -mediated oxidative insult in H9C2 myocardial cells. Biochim Biophys Acta 2007; 1767(3): 222-32.
[http://dx.doi.org/10.1016/j.bbabio.2007.01.023] [PMID: 17346667]
[250]
Cheema Y, Sherrod JN, Zhao W, et al. Mitochondriocentric pathway to cardiomyocyte necrosis in aldosteronism: Cardioprotective responses to carvedilol and nebivolol. J Cardiovasc Pharmacol 2011; 58(1): 80-6.
[http://dx.doi.org/10.1097/FJC.0b013e31821cd83c] [PMID: 21558884]
[251]
Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Sao Paulo Med J 2015; 133(2): 164-5.
[http://dx.doi.org/10.1590/1516-3180.20151332T1] [PMID: 26018887]
[252]
Sanbe A, Tanonaka K, Kobayasi R, Takeo S. Effects of long-term therapy with ACE inhibitors, captopril, enalapril and trandolapril, on myocardial energy metabolism in rats with heart failure following myocardial infarction. J Mol Cell Cardiol 1995; 27(10): 2209-22.
[http://dx.doi.org/10.1016/S0022-2828(95)91551-6] [PMID: 8576937]
[253]
de Cavanagh EMV, Toblli JE, Ferder L, Piotrkowski B, Stella I, Inserra F. Renal mitochondrial dysfunction in spontaneously hypertensive rats is attenuated by losartan but not by amlodipine. Am J Physiol Regul Integr Comp Physiol 2006; 290(6): R1616-25.
[http://dx.doi.org/10.1152/ajpregu.00615.2005] [PMID: 16410402]
[254]
Vogiatzi G, Oikonomou E, Siasos G, et al. Statins and inflammation in cardiovascular disease. Curr Pharm Des 2017.
[http://dx.doi.org/10.2174/1381612823666171009141201]
[255]
Tousoulis D, Oikonomou E, Siasos G, et al. Dose-dependent effects of short term atorvastatin treatment on arterial wall properties and on indices of left ventricular remodeling in ischemic heart failure. Atherosclerosis 2013; 227(2): 367-72.
[http://dx.doi.org/10.1016/j.atherosclerosis.2013.01.015] [PMID: 23433403]
[256]
Costa S, Reina-Couto M, Albino-Teixeira A, Sousa T. Statins and oxidative stress in chronic heart failure. Rev Port Cardiol 2016; 35(1): 41-57.
[http://dx.doi.org/10.1016/j.repc.2015.09.006] [PMID: 26763895]
[257]
Parihar A, Parihar MS, Zenebe WJ, Ghafourifar P. Statins lower calcium-induced oxidative stress in isolated mitochondria. Hum Exp Toxicol 2012; 31(4): 355-63.
[http://dx.doi.org/10.1177/0960327111429141] [PMID: 22144727]
[258]
Tousoulis D, Koniari K, Antoniades C, et al. Combined effects of atorvastatin and metformin on glucose-induced variations of inflammatory process in patients with diabetes mellitus. Int J Cardiol 2011; 149(1): 46-9.
[http://dx.doi.org/10.1016/j.ijcard.2009.11.038] [PMID: 20034685]
[259]
Cahova M, Palenickova E, Dankova H, et al. Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation. Am J Physiol Gastrointest Liver Physiol 2015; 309(2): G100-11.
[http://dx.doi.org/10.1152/ajpgi.00329.2014] [PMID: 26045616]
[260]
Hauner H. The mode of action of thiazolidinediones. Diabetes Metab Res Rev 2002; 18(Suppl. 2): S10-5.
[http://dx.doi.org/10.1002/dmrr.249] [PMID: 11921433]
[261]
Hernanz R, Martín Á, Pérez-Girón JV, et al. Pioglitazone treatment increases COX-2-derived prostacyclin production and reduces oxidative stress in hypertensive rats: Role in vascular function. Br J Pharmacol 2012; 166(4): 1303-19.
[http://dx.doi.org/10.1111/j.1476-5381.2012.01825.x] [PMID: 22220498]
[262]
Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. Br J Pharmacol 2014; 171(8): 2029-50.
[http://dx.doi.org/10.1111/bph.12461] [PMID: 24117165]
[263]
Sabbah HN, Gupta RC, Kohli S, Wang M, Hachem S, Zhang K. Chronic therapy with elamipretide (MTP-131), a novel mitochondria-targeting peptide, improves left ventricular and mitochondrial function in dogs with advanced heart failure. Circ Heart Fail 2016; 9(2)e002206
[http://dx.doi.org/10.1161/CIRCHEARTFAILURE.115.002206] [PMID: 26839394]
[264]
Daubert MA, Yow E, Dunn G, et al. Novel mitochondria-targeting peptide in heart failure treatment: A randomized, placebo-controlled trial of elamipretide. Circ Heart Fail 2017; 10(12)e004389
[http://dx.doi.org/10.1161/CIRCHEARTFAILURE.117.004389] [PMID: 29217757]
[265]
See F, Thomas W, Way K, et al. p38 mitogen-activated protein kinase inhibition improves cardiac function and attenuates left ventricular remodeling following myocardial infarction in the rat. J Am Coll Cardiol 2004; 44(8): 1679-89.
[http://dx.doi.org/10.1016/j.jacc.2004.07.038] [PMID: 15489104]

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