Apoptosis in ischemic heart disease

. 2017 May 01 ; 15 (1) : 87. [epub] 20170501

Jazyk angličtina Země Velká Británie, Anglie Médium electronic

Typ dokumentu časopisecké články, přehledy

Perzistentní odkaz   https://www.medvik.cz/link/pmid28460644
Odkazy

PubMed 28460644
PubMed Central PMC5412049
DOI 10.1186/s12967-017-1191-y
PII: 10.1186/s12967-017-1191-y
Knihovny.cz E-zdroje

Apoptosis plays an important role in the myocardial loss after acute myocardial infarction and participates in the process of subsequent left ventricular remodeling and development of symptomatic heart failure. Finding a sensitive apoptotic marker that would help in prognostic stratification of patients after acute myocardial infarction and offer new therapeutic strategies is thus of a great importance. Several studies suggest that tumor necrosis factor-related apoptosis inducing ligand (TRAIL) represents a very promising marker of prognosis in patients with acute myocardial infarction. This review article provides an overview of current knowledge on the role of apoptosis in ischemic heart disease and highlights potentially beneficial apoptotic markers in clinical practice.

Zobrazit více v PubMed

Chen J, Hsieh AF, Dharmarajan K, Masoudi FA, Krumholz HM. National trends in heart failure hospitalization after acute myocardial infarction for Medicare beneficiaries: 1998–2010. Circulation. 2013;128(24):2577–2584. doi: 10.1161/CIRCULATIONAHA.113.003668. PubMed DOI PMC

Abbate A, Biondi-Zoccai GG, Bussani R, Dobrina A, Camilot D, Feroce F, Rossiello R, Baldi F, Silvestri F, Biasucci LM, Baldi A. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. J Am Coll Cardiol. 2003;41(5):753–760. doi: 10.1016/S0735-1097(02)02959-5. PubMed DOI

Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer. 1972;26(4):239–257. doi: 10.1038/bjc.1972.33. PubMed DOI PMC

Brill A, Torchinsky A, Carp H, Toder V. The role of apoptosis in normal and abnormal embryonic development. J Assist Reprod Genet. 1999;16(10):512–519. doi: 10.1023/A:1020541019347. PubMed DOI PMC

Renehan AG, Booth C, Potten CS. What is apoptosis, and why is it important? BMJ. 2001;322(7301):1536–1538. doi: 10.1136/bmj.322.7301.1536. PubMed DOI PMC

Tower J. Programmed cell death in aging. Ageing Res Rev. 2015;23(Pt A):90–100. doi: 10.1016/j.arr.2015.04.002. PubMed DOI PMC

Cotter TG. Apoptosis and cancer: the genesis of a research field. Nat Rev Cancer. 2009;9(7):501–507. doi: 10.1038/nrc2663. PubMed DOI

Cummins NW, Badley AD. Mechanisms of HIV-associated lymphocyte apoptosis: 2010. Cell Death Dis. 2010;1:e99. doi: 10.1038/cddis.2010.77. PubMed DOI PMC

Roulston A, Marcellus RC, Branton PE. Viruses and apoptosis. Annu Rev Microbiol. 1999;53:577–628. doi: 10.1146/annurev.micro.53.1.577. PubMed DOI

Worth A, Thrasher AJ, Gaspar HB. Autoimmune lymphoproliferative syndrome: molecular basis of disease and clinical phenotype. Br J Haematol. 2006;133(2):124–140. doi: 10.1111/j.1365-2141.2006.05993.x. PubMed DOI

Lev N, Melamed E, Offen D. Apoptosis and Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 2003;27(2):245–250. doi: 10.1016/S0278-5846(03)00019-8. PubMed DOI

Mines MA, Beurel E, Jope RS. Regulation of cell survival mechanisms in Alzheimer’s disease by glycogen synthase kinase-3. Int J Alzheimers Dis. 2011;2011:861072. PubMed PMC

Sawa A, Wiegand GW, Cooper J, Margolis RL, Sharp AH, Lawler JF, Jr, Greenamyre JT, Snyder SH, Ross CA. Increased apoptosis of Huntington disease lymphoblasts associated with repeat length-dependent mitochondrial depolarization. Nat Med. 1999;5(10):1194–1198. doi: 10.1038/13518. PubMed DOI

Saraste A, Pulkki K, Kallajoki M, et al. Apoptosis in human acute myocardial infarction. Circulation. 1997;95:320–323. doi: 10.1161/01.CIR.95.2.320. PubMed DOI

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;28:2005–2016. doi: 10.1006/jmcc.1996.0193. PubMed DOI

Abbate A, Melfi R, Patti G, et al. Apoptosis in recent myocardial infarction. Clin Ter. 2000;151:247–251. PubMed

Baldi A, Abbate A, Bussani R, Patti G, Melfi R, Angelini A, Dobrina A, Rossiello R, Silvestri F, Baldi F, Di Sciascio G. Apoptosis and post-infarction left ventricular remodeling. J Mol Cell Cardiol. 2002;34(2):165–174. doi: 10.1006/jmcc.2001.1498. PubMed DOI

Ashkenazi A, Dixit VM. Death receptors: signaling and modulation. Science. 1998;281:1305–1308. doi: 10.1126/science.281.5381.1305. PubMed DOI

Lee P, Sata M, Lefer DJ, Factor SM, Walsh K, et al. Fas pathway is a critical mediator of cardiac myocyte death and MI during ischemia-reperfusion in vivo. Am J Physiol Heart Circ Physiol. 2003;284:H456–H463. doi: 10.1152/ajpheart.00777.2002. PubMed DOI

Ohtsuka T, Hamada M, Sasaki O, et al. Clinical implications of circulating soluble Fas and Fas ligand in patients with acute myocardial infarction. Coron Artery Dis. 1999;10:221–225. doi: 10.1097/00019501-199906000-00003. PubMed DOI

Fertin M, Bauters A, Pinet F, et al. Circulating levels of soluble Fas ligand and left ventricular remodeling after acute myocardial infarction (from the REVE-2 study) J Cardiol. 2012;60:93–97. doi: 10.1016/j.jjcc.2012.03.001. PubMed DOI

Nilsson L, Szymanowski A, Swahn E, et al. Soluble TNF receptors are associated with infarct size and ventricular dysfunction in ST-elevation myocardial infarction. PLoS ONE. 2013;8(2):e55477. doi: 10.1371/journal.pone.0055477. PubMed DOI PMC

Osmancik P, Teringova E, Tousek P, et al. Prognostic value of TNF-related apoptosis inducing ligand (TRAIL) in acute coronary syndrome patients. PLoS ONE. 2013;8(2):e53860. doi: 10.1371/journal.pone.0053860. PubMed DOI PMC

Kawakami H, Shigematsu Y, Ohtsuka T, et al. Increased circulating soluble form of Fas in patients with dilated cardiomyopathy. Jpn Circ J. 1998;62:873–876. doi: 10.1253/jcj.62.873. PubMed DOI

Niessner A, Hohensinner PJ, Rychli K, et al. Prognostic value of apoptosis markers in advanced heart failure patients. Eur Heart J. 2009;30(7):789–796. doi: 10.1093/eurheartj/ehp004. PubMed DOI

Tsutamoto T, Wada A, Maeda K, et al. Relationship between plasma levels of cardiac natriuretic peptides and soluble Fas: plasma soluble Fas as a prognostic predictor in patients with congestive heart failure. J Card Fail. 2001;7(4):322–328. doi: 10.1054/jcaf.2001.30134. PubMed DOI

Krown KA, Page MT, Nguyen C, Zechner D, Gutierrez V, Comstock KL, Glembotski CC, Quintana PJ, Sabbadini RA. Tumor necrosis factor α-induced apoptosis in cardiac myocytes. Involvement of the sphingolipid signaling cascade in cardiac cell death. J Clin Investig. 1996;98(12):2854–2865. doi: 10.1172/JCI119114. PubMed DOI PMC

Asgeri M, Pourafkari L, Kundra A, Javadzadegan H, Negargar S, Nader ND. Dual effects of tumor necrosis factor alpha on myocardial injury following prolonged hypoperfusion of the heart. Immunol Investig. 2015;44(1):23–35. doi: 10.3109/08820139.2014.921689. PubMed DOI

Monden Y, Kubota T, Inoue T, Tsutsumi T, Kawano S, Ide T, Tsutsui H, Sunagawa K. Tumor necrosis factor-alpha is toxic via receptor 1 and protective via receptor 2 in a murine model of myocardial infarction. Am J Physiol Heart Circ Physiol. 2007;293(1):H743–H753. doi: 10.1152/ajpheart.00166.2007. PubMed DOI

Doyama K, Fujiwara H, Fukumoto M, et al. Tumour necrosis factor is expressed in cardiac tissues of patients with heart failure. Int J Cardiol. 1996;54:217–225. doi: 10.1016/0167-5273(96)02607-1. PubMed DOI

Torre-Amione G, Kapadia S, Lee J, et al. Tumor necrosis factor-alpha and tumor necrosis factor receptors in the failing human heart. Circulation. 1996;93:704–711. doi: 10.1161/01.CIR.93.4.704. PubMed DOI

Mann DL, McMurray JJ, Packer M, Swedberg K, Borer JS, Colucci WS, Djian J, Drexler H, Feldman A, Kober L, Krum H, Liu P, Nieminen M, Tavazzi L, van Veldhuisen DJ, Waldenstrom A, Warren M, Westheim A, Zannad F, Fleming T. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL) Circulation. 2004;109(13):1594–1602. doi: 10.1161/01.CIR.0000124490.27666.B2. PubMed DOI

Chung ES, Packer M, Lo KH, Fasanmade AA, Willerson JT. Randomized, double-blind, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-α, in patients with moderate-to-severe heart failure: results of the anti-TNF therapy against congestive heart failure (ATTACH) trial. Circulation. 2003;107(25):3133–3140. doi: 10.1161/01.CIR.0000077913.60364.D2. PubMed DOI

Kehmeier ES, Lepper W, Kropp M, Heiss C, Hendgen-Cotta U, Balzer J, Neizel M, Meyer C, Merx MW, Verde PE, Ohmann C, Heusch G, Kelm M, Rassaf T. TNF-α, myocardial perfusion and function in patients with ST-segment elevation myocardial infarction and primary percutaneous coronary intervention. Clin Res Cardiol. 2012;101(10):815–827. doi: 10.1007/s00392-012-0465-x. PubMed DOI

Mielczarek-Palacz A, Sikora J, Kondera-Anasz Z, Smycz M. Changes in concentrations of tumor necrosis factor TNF and its soluble receptors type 1 (sTNF-r1) and type 2 (sTNF-R2) in serum of patients with ST-segment elevation myocardial infarction. Wiad Lek. 2011;64(2):71–74. PubMed

Valgimigli M, Ceconi C, Malagutti P, Merli E, Soukhomovskaia O, Francolini G, Cicchitelli G, Olivares A, Parrinello G, Percoco G, Guardigli G, Mele D, Pirani R, Ferrari R. Tumor necrosis factor-alpha receptor 1 is a major predictor of mortality and new-onset heart failure in patients with acute myocardial infarction: the cytokine-activation and long-term prognosis in myocardial infarction (C-ALPHA) study. Circulation. 2005;111(7):863–870. doi: 10.1161/01.CIR.0000155614.35441.69. PubMed DOI

Ueland T, Kjekshus J, Frøland SS, Omland T, Squire IB, Gullestad L, Dickstein K, Aukrust P. Plasma levels of soluble tumor necrosis factor receptor type I during the acute phase following complicated myocardial infarction predicts survival in high-risk patients. J Am Coll Cardiol. 2005;46(11):2018–2021. doi: 10.1016/j.jacc.2005.08.039. PubMed DOI

Gonzálvez M, Ruiz-Ros JA, Pérez-Paredes M, Lozano ML, García-Almagro FJ, Martínez-Corbalán F, Giménez DM, Carrillo A, Carnero A, Cubero T, Gonzálvez JJ, Ureña I, Vicente V. Prognostic value of tumor necrosis factor-alpha in patients with ST-segment elevation acute myocardial infarction. Rev Esp Cardiol. 2007;60(12):1233–1241. doi: 10.1157/13113928. PubMed DOI

Kaya EB, Ozer N, Deveci OS, Kepez A, Tülümen E, Aksöyek S, Atalar E, Ovünç K, Ozmen F, Ozkutlu H. The early predictors of ventricular remodeling after myocardial infarction: the role of tumor necrosis factor-alpha. Anadolu Kardiyol Derg. 2009;9(2):84–90. PubMed

Lin XM, Zhang ZY, Wang LF, Zhang L, Liu Y, Liu XL, Yang XC, Cui L, Zhang L. Attenuation of tumor necrosis factor-alpha elevation and improved heart function by postconditioning for 60 seconds in patients with acute myocardial infarction. Chin Med J. 2010;123(14):1833–1839. PubMed

Padfield GJ, Din JN, Koushiappi E, Mills NL, Robinson SD, Cruden Nle M, Lucking AJ, Chia S, Harding SA, Newby DE. Cardiovascular effects of tumour necrosis factor α antagonism in patients with acute myocardial infarction: a first in human study. Heart. 2013;99(18):1330–1335. doi: 10.1136/heartjnl-2013-303648. PubMed DOI PMC

Huangfu F, Zhao X, Wang X, Tang L, Jiang J. There is no association between TNF-α gene polymorphisms and the risk of coronary artery heart disease: a meta-analysis of 8351 cases and 8423 controls. J Cardiovasc Surg (Torino). 2016. [Epub ahead of print]. PubMed

Suliman A, Lam A, Datta R, Srivastava RK. Intracellular mechanisms of TRAIL: apoptosis through mitochondrial-dependent and -independent pathways. Oncogene. 2001;20:2122–2133. doi: 10.1038/sj.onc.1204282. PubMed DOI

Wiley SR, Schooley K, Smolak PJ, Din WS, Huang CP, Nicholl JK, Sutherland GR, Smith TD, Rauch C, Smith CA, et al. Identification and characterization of a new member of the TNF family that induces apoptosis. Immunity. 1995;3(6):673–682. doi: 10.1016/1074-7613(95)90057-8. PubMed DOI

Jeremias I, Kupatt C, Martin-Villalba A, Habazettl H, Schenkel J, Boekstegers P, Debatin KM. Involvement of CD95/Apo1/Fas in cell death after myocardial ischemia. Circulation. 2000;102(8):915–920. doi: 10.1161/01.CIR.102.8.915. PubMed DOI

LeBlanc HN, Ashkenazi A. Apo2L/TRAIL and its death and decoy receptors. Cell Death Differ. 2003;10:66–75. doi: 10.1038/sj.cdd.4401187. PubMed DOI

Toffoli B, Bernardi S, Candido R, Zacchigna S, Fabris B, Secchiero P. TRAIL shows potential cardioprotective activity. Investig New Drugs. 2012;30(3):1257–1260. doi: 10.1007/s10637-010-9627-8. PubMed DOI

Secchiero P, Candido R, Corallini F, Zacchigna S, Toffoli B, Rimondi E, Fabris B, Giacca M, Zauli G. Systemic tumor necrosis factor-related apoptosis-inducing ligand delivery shows antiatherosclerotic activity in apolipoprotein E-null diabetic mice. Circulation. 2006;114(14):1522–1530. doi: 10.1161/CIRCULATIONAHA.106.643841. PubMed DOI

Mori K, Ikari Y, Jono S, Shioi A, Ishimura E, Emoto M, Inaba M, Hara K, Nishizawa Y. Association of serum TRAIL level with coronary artery disease. Thromb Res. 2010;125(4):322–325. doi: 10.1016/j.thromres.2009.11.024. PubMed DOI

Secchiero P, Corallini F, Ceconi C, Parrinello G, Volpato S, Ferrari R, Zauli G. Potential prognostic significance of decreased serum levels of TRAIL after acute myocardial infarction. PLoS ONE. 2009;4(2):e4442. doi: 10.1371/journal.pone.0004442. PubMed DOI PMC

Volpato S, Ferrucci L, Secchiero P, Corallini F, Zuliani G, Fellin R, Guralnik JM, Bandinelli S, Zauli G. Association of tumor necrosis factor-related apoptosis-inducing ligand with total and cardiovascular mortality in older adults. Atherosclerosis. 2011;215(2):452–458. doi: 10.1016/j.atherosclerosis.2010.11.004. PubMed DOI PMC

Secchiero P, Gonelli A, Corallini F, Ceconi C, Ferrari R, Zauli G. Metalloproteinase 2 cleaves in vitro recombinant TRAIL: potential implications for the decreased serum levels of TRAIL after acute myocardial infarction. Atherosclerosis. 2010;211(1):333–336. doi: 10.1016/j.atherosclerosis.2010.02.024. PubMed DOI

Youle RJ, Strasser A. The BCL-2 protein family: opposing activities that mediate cell death. Nat Rev Mol Cell Biol. 2008;9:47–59. doi: 10.1038/nrm2308. PubMed DOI

Brocheriou V, Hagege AA, Oubenaissa A, et al. Cardiac functional improvement by a human Bcl-2 transgene in a mouse model of ischemia/reperfusion injury. J Gene Med. 2000;2:326–333. doi: 10.1002/1521-2254(200009/10)2:5<326::AID-JGM133>3.0.CO;2-1. PubMed DOI

Chen Z, Chua CC, Ho YS, Hamdy RC, Chua BH. Overexpression of Bcl-2 attenuates apoptosis and protects against myocardial I/R injury in transgenic mice. Am J Physiol Heart Circ Physiol. 2001;280:H2313–H2320. PubMed

Misao J, Hayakawa Y, Ohno M, et al. Expression of bcl-2 protein, an inhibitor of apoptosis, and Bax, an accelerator of apoptosis, in ventricular myocytes of human hearts with myocardial infarction. Circulation. 1996;94:1506–1512. doi: 10.1161/01.CIR.94.7.1506. PubMed DOI

Alireza A, Raheleh S, Abbass R, Mojgan M, Mohamadreza M, Gholamreza M, Shadi B. An immunohistochemistry study of tissue bcl-2 expression and its serum levels in breast cancer patients. Ann N Y Acad Sci. 2008;1138:114–120. doi: 10.1196/annals.1414.017. PubMed DOI

Fadok VA, de Cathelineau A, Daleke DL, Henson PM, Bratton DL. Loss of phospholipid asymmetry and surface exposure of phosphatidylserine is required for phagocytosis of apoptotic cells by macrophages and fibroblasts. J Biol Chem. 2001;276:1071–1077. doi: 10.1074/jbc.M003649200. PubMed DOI

Condorelli G, Roncarati R, Ross J, Jr, et al. Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function. Proc Natl Acad Sci USA. 2001;98:9977–9982. doi: 10.1073/pnas.161120198. PubMed DOI PMC

Liu Q. Lentivirus mediated interference of caspase-3 expression ameliorates the heart function on rats with acute myocardial infarction. Eur Rev Med Pharmacol Sci. 2014;18(13):1852–1858. PubMed

Agosto M, Azrin M, Singh K, Jaffe AS, Liang BT. Serum caspase-3 p17 fragment is elevated in patients with ST-segment elevation myocardial infarction: a novel observation. J Am Coll Cardiol. 2011;57(2):220–221. doi: 10.1016/j.jacc.2010.08.628. PubMed DOI

Wu JJ, Poon KY, Bebchuk JD. Association between the type and length of tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. J Drugs Dermatol. 2013;12(8):899–903. PubMed

Armstrong AW. Do TNF inhibitors reduce the risk of myocardial infarction in psoriasis patients? JAMA. 2013;309(19):2043–2044. doi: 10.1001/jama.2013.4695. PubMed DOI

Dixon WG, Watson KD, Lunt M, Hyrich KL, British Society for Rheumatology Biologics Register Control Centre Consortium. Silman AJ, Symmons DP, British Society for Rheumatology Biologics Register Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti-tumor necrosis factor alpha therapy: results from the British Society for Rheumatology Biologics Register. Arthritis Rheum. 2007;56(9):2905–2912. doi: 10.1002/art.22809. PubMed DOI PMC

Barnabe C, Martin BJ, Ghali WA. Systematic review and meta-analysis: anti-tumor necrosis factor α therapy and cardiovascular events in rheumatoid arthritis. Arthritis Care Res. 2011;63(4):522–529. doi: 10.1002/acr.20371. PubMed DOI

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...