Abstract
Ischemic heart disease (IHD) due to reduced coronary blood flow over a prolonged period as well as reperfusion of the ischemic myocardium are associated with irreversible cellular damage and contractile failure. Although several major mechanisms including inflammation, oxidative stress and intracellular Ca2+-overload have been identified to induce cardiac injury in IHD, the occurrence of cardiomyocyte cell death due to apoptosis has been considered to play a critical role in the development of heart dysfunction. The activation of several apoptotic and anti-apoptotic proteins belonging to both extrinsic and intrinsic pathways of apoptosis has been demonstrated in IHD. Some major proteins of the extrinsic apoptotic pathway include Fas/Fas ligand, TNF-α, TRAIL as well as Caspase-8 and Caspase-10. On the other hand, mediator proteins of the intrinsic apoptotic pathway are: Bcl-2, Bax, Cytochrome C and Caspase-9. Both extrinsic and intrinsic pathways converge on the terminal apoptotic pathway in which different proteins such as Caspase-3, Caspase-6 and Caspase-7 are activated leading to the degradation of cellular constituents in the ischemic myocardium. Although several agents targeting different apoptotic proteins have been shown to exert cardioprotective effects in experimental studies, the results in various clinical trials in IHD have not been encouraging.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Bartekova M, Barancik M, Dhalla NS (2016) Role of oxidative stress in subcellular defects in ischemic heart disease. In: Gelpi RJ, Boveris A, Paderosa JJ (eds) Biochemistry of oxidative stress: physiopathology and clinical aspects; Adv Biochem Health Dis 16: 129–146
Bartekova M, Ferenczyova K, Jelemensky M, Dhalla NS (2019) Role of oxidative stress and cardiovascular risk factors in ischemic heart disease. In: Chakraborti S, Dhalla NS, Ganguly NK, Dikshit M (eds) Oxidative stress in heart diseases. Springer Nature Singapore, pp 375–394. ISBN 978-981-13-8272-7
Schaftenaar F, Frodermann V, Kuiper J, Lutgens E (2016) Atherosclerosis: the interplay between lipids and immune cells. Curr Opin Lipidol 27(3):209–215. https://doi.org/10.1097/MOL.0000000000000302
Geovanini GR, Libby P (2018) Atherosclerosis and inflammation: overview and updates. Clin Sci (Lond) 132(12):1243–1252. https://doi.org/10.1042/CS20180306
Bartekova M, Radosinska J, Jelemensky M, Dhalla NS (2018) Role of cytokines and inflammation in heart function during health and disease. Heart Fail Rev 23(5):733–758. https://doi.org/10.1007/s10741-018-9716-x
Wu MY, Yiang GT, Liao WT et al (2018) Current mechanistic concepts in ischemia and reperfusion injury. Cell Physiol Biochem 46(4):1650–1667. https://doi.org/10.1159/000489241
Zaman S, Wang R, Gandhi V (2014) Targeting the apoptosis pathway in hematologic malignancies. Leuk Lymphoma 55(9):1980–1992. https://doi.org/10.3109/10428194.2013.855307
Cotter TG (2009) Apoptosis and cancer: the genesis of a research field. Nat Rev Cancer 9(7):501–507. https://doi.org/10.1038/nrc2663
Lev N, Melamed E, Offen D (2003) Apoptosis and Parkinson’s disease. Prog Neuropsychopharmacol Biol Psychiat 27(2):245–250
Mines MA, Beurel E, Jope RS (2011) Regulation of cell survival mechanisms in Alzheimer's disease by glycogen synthase kinase-3. Int J Alzheimers Dis 2011:861072. https://doi.org/10.4061/2011/861072
Roulston A, Marcellus RC, Branton PE (1999) Viruses and apoptosis. Annu Rev Microbiol 53:577–628
Wang L, Wang FS, Gershwin ME (2015) Human autoimmune diseases: a comprehensive update. J Intern Med 278(4):369–395. https://doi.org/10.1111/joim.12395
Mihaljevic O, Zivancevic-Simonovic S, Milosevic-Djordjevic O et al (2018) Apoptosis and genome instability in children with autoimmune diseases. Mutagenesis 33(5–6):351–357. https://doi.org/10.1093/mutage/gey037
Teringova E, Tousek P (2017) Apoptosis in ischemic heart disease. J Transl Med 15(1):87. https://doi.org/10.1186/s12967-017-1191-y
Olivetti G, Quaini F, Sala R et al (1996) 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 28(9):2005–2016
Saraste A, Pulkki K, Kallajoki M et al (1997) Apoptosis in human acute myocardial infarction. Circulation 95(2):320–323
Baldi A, Abbate A, Bussani R et al (2002) Apoptosis and post-infarction left ventricular remodeling. J Mol Cell Cardiol 34(2):165–174
Lee P, Sata M, Lefer DJ et al (2003) Fas pathway is a critical mediator of cardiac myocyte death and MI during ischemia-reperfusion in vivo. Am J Physiol Heart Circ Physiol 284(2):H456–H463
Liu XM, Yang ZM, Liu XK (2017) Fas/FasL induces myocardial cell apoptosis in myocardial ischemia-reperfusion rat model. Eur Rev Med Pharmacol Sci 21(12):2913–2918
Li Y, Takemura G, Kosai K et al (2004) Critical roles for the Fas/Fas ligand system in postinfarction ventricular remodeling and heart failure. Circ Res 95(6):627–636
Fertin M, Bauters A, Pinet F, Bauters C (2012) Circulating levels of soluble Fas ligand and left ventricular remodeling after acute myocardial infarction (from the REVE-2 study). J Cardiol 60(2):93–97. https://doi.org/10.1016/j.jjcc.2012.03.001
Nilsson L, Szymanowski A, Swahn E, Jonasson L (2013) Soluble TNF receptors are associated with infarct size and ventricular dysfunction in ST-elevation myocardial infarction. PLoS One 8(2):e55477. https://doi.org/10.1371/journal.pone.0055477
Osmancik P, Teringova E, Tousek P et al (2013) Prognostic value of TNF-related apoptosis inducing ligand (TRAIL) in acute coronary syndrome patients. PLoS One 8(2):e53860. https://doi.org/10.1371/journal.pone.0053860
Tekin D, Xi L, Kukreja RC (2006) Genetic deletion of Fas receptors or Fas ligands does not reduce infarct size after acute global ischemia-reperfusion in isolated mouse heart. Cell Biochem Biophys 44(1):111–117
Sahinarslan A, Boyaci B, Kocaman SA et al (2012) The relationship of serum soluble Fas ligand (sFasL) level with the extent of coronary artery disease. Int J Angiol 21(1):29–34. https://doi.org/10.1055/s-0032-1306418
Kawakami H, Shigematsu Y, Ohtsuka T et al (1998) Increased circulating soluble form of Fas in patients with dilated cardiomyopathy. Jpn Circ J 62(12):873–876
Tsutamoto T, Wada A, Maeda K et al (2001) 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 7(4):322–328
Niessner A, Hohensinner PJ, Rychli K et al (2009) Prognostic value of apoptosis markers in advanced heart failure patients. Eur Heart J 30(7):789–796. https://doi.org/10.1093/eurheartj/ehp004
Fan Q, Huang ZM, Boucher M et al (2013) Inhibition of Fas-associated death domain-containing protein (FADD) protects against myocardial ischemia/reperfusion injury in a heart failure mouse model. PLoS One 8(9):e73537. https://doi.org/10.1371/journal.pone.0073537
Saini HK, Xu YJ, Zhang M, Liu PP, Kirshenbaum LA, Dhalla NS (2005) Role of tumour necrosis factor-alpha and other cytokines in ischemia-reperfusion-induced injury in the heart. Exp Clin Cardiol 10(4):213–222
Zhang M, Xu YJ, Saini HK et al (2005) TNF-alpha as a potential mediator of cardiac dysfunction due to intracellular Ca2+-overload. Biochem Biophys Res Commun 327(1):57–63
Zhang M, Xu YJ, Saini HK et al (2005) Pentoxifylline attenuates cardiac dysfunction and reduces TNF-alpha level in ischemic-reperfused heart. Am J Physiol Heart Circ Physiol 289(2):H832-839
Zhou CN, Yao W, Gong YN et al (2019) 22-oxacalcitriol protects myocardial ischemia-reperfusion injury by suppressing NF-κB/TNF-α pathway. Eur Rev Med Pharmacol Sci 23(12):5495–5502. https://doi.org/10.26355/eurrev_201906_18219
Huang XW, Pan MD, Du PH, Wang LX (2018) Arginase-2 protects myocardial ischemia-reperfusion injury via NF-κB/TNF-α pathway. Eur Rev Med Pharmacol Sci 22(19):6529–6537. https://doi.org/10.26355/eurrev_201810_16067
Meldrum DR (1998) Tumor necrosis factor in the heart. Am J Physiol Regul Integr Comp Physiol 274:R577–R595
Bajaj G, Sharma RK (2006) TNF-alpha-mediated cardiomyocyte apoptosis involves caspase-12 and calpain. Biochem Biophys Res Commun 345(4):1558–1564
Jarrah AA, Schwarskopf M, Wang ER et al (2018) SDF-1 induces TNF-mediated apoptosis in cardiac myocytes. Apoptosis 23(1):79–91. https://doi.org/10.1007/s10495-017-1438-3
Asgeri M, Pourafkari L, Kundra A et al (2015) Dual effects of tumor necrosis factor alpha on myocardial injury following prolonged hypoperfusion of the heart. Immunol Investig 44(1):23–35
Monden Y, Kubota T, Inoue T et al (2007) 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 293(1):H743–H753
Kleinbongard P, Heusch G, Schulz R (2010) TNF alpha in atherosclerosis, myocardial ischemia/reperfusion and heart failure. Pharmacol Ther 127(3):295–314. https://doi.org/10.1016/j.pharmthera.2010.05.002
Jeremias I, Kupatt C, Martin-Villalba A et al (2000) Involvement of CD95/Apo1/Fas in cell death after myocardial ischemia. Circulation 102(8):915–920
LeBlanc HN, Ashkenazi A (2003) Apo2L/TRAIL and its death and decoy receptors. Cell Death Differ 10:66–75
Di Bartolo BA, Cartland SP, Prado-Lourenco L et al (2015) Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes angiogenesis and ischemia-induced neovascularization via NADPH oxidase 4 (NOX4) and nitric oxide-dependent mechanisms. J Am Heart Assoc 4(11)pii: e002527. https://doi.org/10.1161/JAHA.115.002527
Nakajima H, Yanase N, Oshima K et al (2003) Enhanced expression of the apoptosis inducing ligand TRAIL in mononuclear cells after myocardial infarction. Jpn Heart J 44(6):833–844
Jiang Y, Chen X, Fan M et al (2017) TRAIL facilitates cytokine expression and macrophage migration during hypoxia/reoxygenation via ER stress-dependent NF-κB pathway. Mol Immunol 82:123–136. https://doi.org/10.1016/j.molimm.2016.12.023
Toffoli B, Bernardi S, Candido R et al (2012) TRAIL shows potential cardioprotective activity. Investig New Drugs 30(3):1257–1260
Secchiero P, Candido R, Corallini F et al (2006) Systemic tumor necrosis factor-related apoptosisinducing ligand delivery shows antiatherosclerotic activity in apolipoprotein E-null diabetic mice. Circulation 114(14):1522–1530
Secchiero P, Corallini F, Ceconi C et al (2009) Potential prognostic significance of decreased serum levels of TRAIL after acute myocardial infarction. PLoS One 4(2):e4442. https://doi.org/10.1371/journal.pone.0004442
Volpato S, Ferrucci L, Secchiero P et al (2011) Association of tumor necrosis factor-related apoptosis-inducing ligand with total and cardiovascular mortality in older adults. Atherosclerosis 215(2):452–458. https://doi.org/10.1016/j.atherosclerosis.2010.11.004
Deftereos S, Giannopoulos G, Kossyvakis C et al (2012) Association of soluble tumour necrosis factor-related apoptosis-inducing ligand levels with coronary plaque burden and composition. Heart 98(3):214–218. https://doi.org/10.1136/heartjnl-2011-300339
Dessein PH, Lopez-Mejias R, Ubilla B et al (2015) TNF-related apoptosis-inducing ligand and cardiovascular disease in rheumatoid arthritis. Clin Exp Rheumatol 33(4):491–497
Teringova E, Kozel M, Knot J et al (2018) Relationship between TRAIL and left ventricular ejection fraction in patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. Biomed Res Int 2018:3709084. https://doi.org/10.1155/2018/3709084
Luz A, Santos M, Magalhães R et al (2017) Soluble TNF-related apoptosis induced ligand (sTRAIL) is augmented by post-conditioning and correlates to infarct size and left ventricle dysfunction in STEMI patients: a substudy from a randomized clinical trial. Heart Vessels 32(2):117–125. https://doi.org/10.1007/s00380-016-0851-9
Kruidering M, Evan GI (2000) Caspase-8 in apoptosis: the beginning of “the end”? IUBMB Life 50(2):85–90
Stephanou A, Brar B, Liao Z et al (2001) Distinct initiator caspases are required for the induction of apoptosis in cardiac myocytes during ischaemia versus reperfusion injury. Cell Death Differ 8(4):434–435
Scarabelli TM, Stephanou A, Pasini E et al (2002) Different signaling pathways induce apoptosis in endothelial cells and cardiac myocytes during ischemia/reperfusion injury. Circ Res 90(6):745–748
Roubille F, Combes S, Leal-Sanchez J et al (2007) Myocardial expression of a dominant-negative form of Daxx decreases infarct size and attenuates apoptosis in an in vivo mouse model of ischemia/reperfusion injury. Circulation 116(23):2709–2717
Lu X, Moore PG, Liu H, Schaefer S (2011) Phosphorylation of ARC is a critical element in the antiapoptotic effect of anesthetic preconditioning. Anesth Analg 112(3):525–531. https://doi.org/10.1213/ANE.0b013e318205689b
Palee S, Weerateerangkul P, Chinda K et al (2013) Mechanisms responsible for beneficial and adverse effects of rosiglitazone in a rat model of acute cardiac ischaemia-reperfusion. Exp Physiol 98(5):1028–1037. https://doi.org/10.1113/expphysiol.2012.070433
Fauconnier J, Meli AC, Thireau J et al (2011) Ryanodine receptor leak mediated by caspase-8 activation leads to left ventricular injury after myocardial ischemia-reperfusion. Proc Natl Acad Sci USA 108(32):13258–13263. https://doi.org/10.1073/pnas.1100286108
Liang Y, Lin Q, Zhu J et al (2014) The caspase-8 shRNA-modified mesenchymal stem cells improve the function of infarcted heart. Mol Cell Biochem 397(1–2):7–16. https://doi.org/10.1007/s11010-014-2165-5
Levine B, Sinha S, Kroemer G (2008) Bcl-2 family members: dual regulators of apoptosis and autophagy. Autophagy 4(5):600–606
Chen Z, Chua CC, Ho YS et al (2001) Overexpression of Bcl-2 attenuates apoptosis and protects against myocardial I/R injury in transgenic mice. Am J Physiol Heart Circ Physiol 280:H2313–H2320
Misao J, Hayakawa Y, Ohno M et al (1996) 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 94:1506–1512
Xing K, Fu X, Jiang L et al (2015) Cardioprotective effect of anisodamine against myocardial ischemia injury and its influence on cardiomyocytes apoptosis. Cell Biochem Biophys 73(3):707–716. https://doi.org/10.1007/s12013-015-0642-4
Li M, Xue L, Sun H, Xu S (2016) Myocardial protective effects of L-Carnitine on ischemia-reperfusion injury in patients with rheumatic valvular heart disease undergoing cardiac surgery. J Cardiothorac Vasc Anesth 30(6):1485–1493. https://doi.org/10.1053/j.jvca.2016.06.006
Hu Q, Luo W, Huang L et al (2016) Apoptosis-related microRNA changes in the right atrium induced by remote ischemic perconditioning during valve replacement surgery. Sci Rep 7(6):18959. https://doi.org/10.1038/srep18959
Zhu LP, Tian T, Wang JY et al (2018) Hypoxia-elicited mesenchymal stem cell-derived exosomes facilitates cardiac repair through miR-125b-mediated prevention of cell death in myocardial infarction. Theranostics 8(22):6163–6177. https://doi.org/10.7150/thno.28021
Liu Y, Yang L, Yin J et al (2018) MicroRNA-15b deteriorates hypoxia/reoxygenation-induced cardiomyocyte apoptosis by downregulating Bcl-2 and MAPK3. J Investig Med 66(1):39–45. https://doi.org/10.1136/jim-2017-000485
Wen Z, Mai Z, Zhu X et al (2020) Mesenchymal stem cell-derived exosomes ameliorate cardiomyocyte apoptosis in hypoxic conditions through microRNA144 by targeting the PTEN/AKT pathway. Stem Cell Res Ther 11(1):36. https://doi.org/10.1186/s13287-020-1563-8
Kura B, Kalocayova B, Devaux Y, Bartekova M (2020) Potential clinical implications of miR-1 and miR-21 in heart disease and cardioprotection. Int J Mol Sci 21(3)pii:700. https://doi.org/10.3390/ijms21030700.
Honda HM, Korge P, Weiss JN (2005) Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci 1047:248–258
Scorrano L, Ashiya M, Buttle K et al (2002) A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis. Dev Cell 2(1):55–67
Korge P, Honda HM, Weiss JN (2003) Effects of fatty acids in isolated mitochondria: implications for ischemic injury and cardioprotection. Am J Physiol Heart Circ Physiol 285(1):H259–H269
Borutaite V, Budriunaite A, Morkuniene R, Brown GC (2001) Release of mitochondrial cytochrome c and activation of cytosolic caspases induced by myocardial ischaemia. Biochim Biophys Acta 1537(2):101–109
Kuznetsov AV, Schneeberger S, Seiler R et al (2004) Mitochondrial defects and heterogeneous cytochrome c release after cardiac cold ischemia and reperfusion. Am J Physiol Heart Circ Physiol 286(5):H1633–H1641
Lundberg KC, Szweda LI (2006) Preconditioning prevents loss in mitochondrial function and release of cytochrome c during prolonged cardiac ischemia/reperfusion. Arch Biochem Biophys 453(1):130–134
Skemiene K, Rakauskaite G, Trumbeckaite S et al (2013) Anthocyanins block ischemia-induced apoptosis in the perfused heart and support mitochondrial respiration potentially by reducing cytosolic cytochrome c. Int J Biochem Cell Biol 45(1):23–29. https://doi.org/10.1016/j.biocel.2012.07.022
Dzhanashiya PKh, Vladytskaya OV, Salibegashvili NV (2004) Efficiency and mechanisms of the antioxidant effect of standard therapy and refracterin in the treatment of chronic heart failure in elderly patients with postinfarction cardiosclerosis. Bull Exp Biol Med 138(4):412–414
Qin F, Liang MC, Liang CS (2005) Progressive left ventricular remodeling, myocyte apoptosis, and protein signaling cascades after myocardial infarction in rabbits. Biochim Biophys Acta 1740(3):499–513
Zeng C, Jiang W, Zheng R et al (2018) Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: role of the apoptotic signaling pathway. PLoS One 13(3):e0193845. https://doi.org/10.1371/journal.pone.0193845
Liu D (2018) Effects of procyanidin on cardiomyocyte apoptosis after myocardial ischemia reperfusion in rats. BMC Cardiovasc Disord 18(1):35. https://doi.org/10.1186/s12872-018-0772-x
Huang LH, Li J, Gu JP et al (2018) Butorphanol attenuates myocardial ischemia reperfusion injury through inhibiting mitochondria-mediated apoptosis in mice. Eur Rev Med Pharmacol Sci 22(6):1819–1824. https://doi.org/10.26355/eurrev_201803_14601
Condorelli G, Roncarati R, Ross J Jr et al (2001) Heart-targeted overexpression of caspase 3 in mice increases infarct size and depresses cardiac function. Proc Natl Acad Sci USA 98:9977–9982
Holly TA, Drincic A, Byun Y et al (1999) Caspase inhibition reduces myocyte cell death induced by myocardial ischemia and reperfusion in vivo. J Mol Cell Cardiol 31(9):1709–1715
Pavo N, Lukovic D, Zlabinger K et al (2017) Intrinsic remote conditioning of the myocardium as a comprehensive cardiac response to ischemia and reperfusion. Oncotarget 8(40):67227–67240. https://doi.org/10.18632/oncotarget.18438
Liu Q (2014) Lentivirus mediated interference of caspase-3 expression ameliorates the heart function on rats with acute myocardial infarction. Eur Rev Med Pharmacol Sci 18(13):1852–1858
Hu S, Yan G, Xu H et al (2014) Hypoxic preconditioning increases survival of cardiac progenitor cells via the pim-1 kinase-mediated anti-apoptotic effect. Circ J 78(3):724–731
You L, Pan YY, An MY et al (2019) The cardioprotective effects of remote ischemic conditioning in a rat model of acute myocardial infarction. Med Sci Monit 25:1769–1779. https://doi.org/10.12659/MSM.914916
Bartekova M, Šimončíková P, Fogarassyová M, Ivanová M et al (2015) Quercetin improves postischemic recovery of heart function in doxorubicin-treated rats and prevents doxorubicin-induced matrix metalloproteinase-2 activation and apoptosis induction. Int J Mol Sci 16(4):8168–8185. https://doi.org/10.3390/ijms16048168
Li C, Wang T, Zhang C et al (2016) Quercetin attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Gene 577(2):275–280. https://doi.org/10.1016/j.gene.2015.12.012
Wang H, Zhao YT, Zhang S et al (2017) Irisin plays a pivotal role to protect the heart against ischemia and reperfusion injury. J Cell Physiol 232(12):3775–3785. https://doi.org/10.1002/jcp.25857
Liu BF, Chen Q, Zhang M, Zhu YK (2019) MiR-124 promotes ischemia-reperfusion induced cardiomyocyte apoptosis by targeting sphingosine kinase 1. Eur Rev Med Pharmacol Sci 23(16):7049–7058. https://doi.org/10.26355/eurrev_201908_18747
Tan H, Qi J, Fan BY et al (2018) MicroRNA-24-3p attenuates myocardial ischemia/reperfusion injury by suppressing RIPK1 expression in mice. Cell Physiol Biochem 51(1):46–62. https://doi.org/10.1159/000495161
Chen Z, Su X, Shen Y et al (2019) MiR322 mediates cardioprotection against ischemia/reperfusion injury via FBXW7/notch pathway. J Mol Cell Cardiol 133:67–74. https://doi.org/10.1016/j.yjmcc.2019.05.020
Saini U, Gumina RJ, Wolfe B et al (2013) Preconditioning mesenchymal stem cells with caspase inhibition and hyperoxia prior to hypoxia exposure increases cell proliferation. J Cell Biochem 114(11):2612–2623. https://doi.org/10.1002/jcb.24609
Knaapen MW, Davies MJ, De Bie M et al (2001) Apoptotic versus autophagic cell death in heart failure. Cardiovasc Res 51(2):304–312
Chapman JG, Magee WP, Stukenbrok HA et al (2002) A novel nonpeptidic caspase-3/7 inhibitor, (S)-(+)-5-[1-(2-methoxymethylpyrrolidinyl)-sulfonyl]isatin reduces myocardial ischemic injury. Eur J Pharmacol 456(1–3):59–68
Zhao L, Zhuang J, Wang Y et al (2019) Propofol ameliorates H9c2 cells apoptosis induced by oxygen glucose geprivation and reperfusion injury via inhibiting high levels of mitochondrial fusion and fission. Front Pharmacol 10:61. https://doi.org/10.3389/fphar.2019.00061
Fischer UM, Tossios P, Huebner A et al (2004) Myocardial apoptosis prevention by radical scavenging in patients undergoing cardiac surgery. J Thorac Cardiovasc Surg 128(1):103–108
Aslanabadi N, Shirzadi HR, Asghari-Soufi H et al (2015) A pilot randomized trial of pentoxifylline for the reduction of periprocedural myocardial injury in patients undergoing elective percutaneous coronary intervention. Eur J Clin Pharmacol 71(2):143–149. https://doi.org/10.1007/s00228-014-1782-y
Mansourian S, Bina P, Fehri A et al (2015) Preoperative oral pentoxifylline in case of coronary artery bypass grafting with left ventricular dysfunction (ejection fraction equal to/less than 30%). Anatol J Cardiol 15(12):1014–1019. https://doi.org/10.5152/akd.2014.5883
Wolfe F, Michaud K (2004) Heart failure in rheumatoid arthritis: rates, predictors, and the effect of anti-tumor necrosis factor therapy. Am J Med 116(5):305–311
Dixon WG, Watson KD, Lunt M et al (2007) 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 56(9):2905–2912
Barnabe C, Martin BJ, Ghali WA (2011) Systematic review and meta-analysis: anti-tumor necrosis factor α therapy and cardiovascular events in rheumatoid arthritis. Arthritis Care Res 63(4):522–529
Wu JJ, Poon KY, Bebchuk JD (2013) Association between the type and length of tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. J Drugs Dermatol 12(8):899–903
Armstrong AW (2013) Do TNF inhibitors reduce the risk of myocardial infarction in psoriasis patients? JAMA 309(19):2043–2044
Mann DL, McMurray JJ, Packer M et al (2004) Targeted anticytokine therapy in patients with chronic heart failure: results of the randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation 109(13):1594–1602
Padfield GJ, Din JN, Koushiappi E et al (2013) Cardiovascular effects of tumour necrosis factor α antagonism in patients with acute myocardial infarction: a first in human study. Heart 99(18):1330–1335
Chung ES, Packer M, Lo KH et al (2003) 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 107(25):3133–3140
Acknowledgements
M.B. is supported by grant from the Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic and the Slovak Academy of Sciences VEGA no. 2/0104/20. The infrastructure support for this project was provided by the St. Boniface Hospital Research Foundation, Winnipeg, Canada.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2022 Springer Nature Switzerland AG
About this chapter
Cite this chapter
Bartekova, M., Shah, A.K., Dhalla, N.S. (2022). Apoptosis in Ischemic Heart Disease. In: Kirshenbaum, L.A. (eds) Biochemistry of Apoptosis and Autophagy. Advances in Biochemistry in Health and Disease, vol 18. Springer, Cham. https://doi.org/10.1007/978-3-030-78799-8_3
Download citation
DOI: https://doi.org/10.1007/978-3-030-78799-8_3
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-030-78798-1
Online ISBN: 978-3-030-78799-8
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)