Apoptosis in heart: Basic mechanisms and implications in cardiovascular diseases

Trends in Molecular Medicine

Volumn 9, Issue 4, 2003, Pages 177-182

  Kang, Peter M ^a   Izumo, Seigo ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

APOPTOSIS; CARDIOVASCULAR DISEASE; HEART; HEART FAILURE; HEART MUSCLE; HEART VENTRICLE HYPERTROPHY; PATHOGENESIS; REVIEW; SIGNAL TRANSDUCTION;

EID: 0038813632     PISSN: 14714914     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1471-4914(03)00025-X     Document Type: Review

References (63)

1. Ohno, M. et al. (1998) 'Apoptotic' myocytes in infarct area in rabbit hearts may be oncotic myocytes with DNA fragmentation: analysis by immunogold electron microscopy combined with in situ nick endlabeling. Circulation 98, 1422-1430
2. Knaapen, M.W. et al. (2001) Apoptotic versus autophagic cell death in heart failure. Cardiovasc. Res. 51, 304-312
3. Klionsky, D.J. and Emr, S.D. (2000) Autophagy as a regulated pathway of cellular degradation. Science 290, 1717-1721
4. Kang, P.M. (2000) Apoptosis and heart failure: a critical review of the literature. Circ. Res. 86, 1107-1113
5. Gottlieb, R.A. et al. (1994) Reperfusion injury induces apoptosis in rabbit cardiomyocytes. J. Clin. Invest. 94, 1621-1628
6. Zheng, T.S. et al. (1999) Caspase knockouts: matters of life and death. Cell Death Differ. 6, 1043-1053
7. Harlin, H. et al. (2001) Characterization of XIAP-deficient mice. Mol. Cell. Biol. 21, 3604-3608
8. Du, C. et al. (2000) Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition. Cell 102, 33-42
9. Koseki, T. et al. (1998) ARC, an inhibitor of apoptosis expressed in skeletal muscle and heart that interacts selectively with caspases. Proc. Natl. Acad. Sci. U. S. A. 95, 5156-5160
10. Ekhterae, D. et al. (1999) ARC inhibits cytochrome c release from mitochondria and protects against hypoxia-induced apoptosis in heartderived H9c2 cells. Circ. Res. 85, e70-e77
11. Li, P.F. et al. (2002) Phosphorylation by protein kinase CK2: a signaling switch for the caspase-inhibiting protein ARC. Mol. Cell 10, 247-258
12. Yaoita, H. et al. (1998) Attenuation of ischemia/reperfusion injury in rats by a caspase inhibitor. Circulation 97, 276-281
13. Laugwitz, K.L. et al. (2001) Blocking caspase-activated apoptosis improves contractility in failing myocardium. Hum. Gene Ther. 12, 2051-2063
14. Nicholson, D.W. (2000) From bench to clinic with apoptosis-based therapeutic agents. Nature 407, 810-816
15. Haunstetter, A. and Izumo, S. (2000) Toward antiapoptosis as a new treatment modality. Circ. Res. 86, 371-376
16. Li, P. et al. (1997) Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell 91, 479-489
17. Adams, J.M. and Cory, S. (1998) The Bcl-2 protein family: arbiters of cell survival. Science 281, 1322-1326
18. Li, H. et al. (1998) Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell 94, 491-501
19. Lindsten, T. et al. (2000) The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. Mol. Cell 6, 1389-1399
20. Misao, J. 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
21. Latif, N. et al. (2000) Upregulation of the Bcl-2 family of proteins in end stage heart failure. J. Am. Coll. Cardiol. 35, 1769-1777
22. Brocheriou, V. et al. (2000) Cardiac functional improvement by a human Bcl-2 transgene in a mouse model of ischemia/reperfusion injury. J. Gene Med. 2, 326-333
23. Maulik, N. et al. (1999) Ischemic preconditioning reduces apoptosis by upregulating anti-death gene Bcl-2. Circulation 100 (Suppl. 19), 369-375
24. Bartling, B. et al. (1999) Myocardial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. Circulation 100 (Suppl. 19), 216-223
25. Nagata, S. (1997) Apoptosis by death factor. Cell 88, 355-365
26. Adachi, M. et al. (1995) Targeted mutation in the Fas gene causes hyperplasia in peripheral lymphoid organs and liver. Nat. Genet. 11, 294-300
27. Takahashi, T. et al. (1994) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76, 969-976
28. Yeh, W.C. et al. (1998) FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis. Science 279, 1954-1958
29. Ishiyama, S. et al. (1998) The Fas/Fas ligand system is involved in the pathogenesis of autoimmune myocarditis in rats. J. Immunol. 161, 4695-4701
30. Twu, C. et al. (2002) Cardiomyocytes undergo apoptosis in human immunodeficiency virus cardiomyopathy through mitochondrion- and death receptor-controlled pathways. Proc. Natl. Acad. Sci. U. S. A. 99, 14386-14391
31. Lee, P. et al. (2003) The Fas pathway is a critical mediator of cardiac myocyte death and myocardial infarction during ischemia/reperfusion in vivo. Am. J. Physiol. Heart Circ. Physiol. 284, H456-H463
32. Irmler, M. et al. (1997) Inhibition of death receptor signals by cellular FLIP. Nature 388, 190-195
33. Kubota, T. et al. (1997) Dilated cardiomyopathy in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-α. Circ. Res. 81, 627-635
34. Nelson, D.P. et al. (2000) Proinflammatory consequences of transgenic Fas ligand expression in the heart. J. Clin. Invest. 105, 1199-1208
35. Rasper, D.M. et al. (1998) Cell death attenuation by 'Usurpin', a mammalian DED-caspase homologue that precludes caspase-8 recruitment and activation by the CD-95 (Fas, APO-1) receptor complex. Cell Death Differ. 5, 271-288
36. αq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proc. Natl. Acad. Sci. U. S. A. 95, 10140-10145
37. Aronow, B.J. et al. (2001) Divergent transcriptional responses to independent genetic causes of cardiac hypertrophy. Physiol Genomics 6, 19-28
38. Yussman, M.G. et al. (2002) Mitochondrial death protein Nix is induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy. Nat. Med. 8, 725-730
39. sα transgenic mice. Circ. Res. 84, 34-42
40. Sheng, Z. et al. (1997) Cardiotrophin 1 (CT-1) inhibition of cardiac myocyte apoptosis via a mitogen-activated protein kinase-dependent pathway. Divergence from downstream CT-1 signals for myocardial cell hypertrophy. J. Biol. Chem. 272, 5783-5791
41. Yasukawa, H. et al. (2001) Suppressor of cytokine signaling-3 is a biomechanical stress-inducible gene that suppresses gp130-mediated cardiac myocyte hypertrophy and survival pathways. J. Clin. Invest. 108, 1459-1467
42. Hirota, H. et al. (1999) Loss of a gp130 cardiac muscle cell survival pathway is a critical event in the onset of heart failure during biomechanical stress. Cell 97, 189-198
43. Lee, W.L. et al. (1999) Insulin-like growth factor I improves cardiovascular function and suppresses apoptosis of cardiomyocytes in dilated cardiomyopathy. Endocrinology 140, 4831-4840
44. Li, Q, et al. (1997) Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy. J. Clin. Invest. 100, 1991-1999
45. Aikawa, R. et al. (2000) Insulin prevents cardiomyocytes from oxidative stress-induced apoptosis through activation of PI3 kinase/Akt. Circulation 102, 2873-2879
46. Matsui, T. et al. (2001) Akt activation preserves cardiac function and prevents injury after transient cardiac ischemia in vivo. Circulation 104, 330-335
47. Datta, S.R. et al. (1997) Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell 91, 231-241
48. Cardone, M.H. et al. (1998) Regulation of cell death protease caspase-9 by phosphorylation. Science 282, 1318-1321
49. Cook, S.A. et al. (1999) Regulation of bcl-2 family proteins during development and in response to oxidative stress in cardiac myocytes: association with changes in mitochondrial membrane potential. Circ. Res. 85, 940-949
50. Fujita, E. et al. (1999) Akt phosphorylation site found in human caspase-9 is absent in mouse caspase-9. Biochem. Biophys. Res. Commun. 264, 550-555
51. Gao, F. et al. (2002) Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemia-reperfusion: the roles of PI3-kinase, Akt, and endothelial nitric oxide synthase phosphorylation. Circulation 105, 1497-1502
52. Aoki, H. et al. (2002) Direct activation of mitochondrial apoptosis machinery by c-Jun N-terminal kinase in adult cardiac myocytes. J. Biol. Chem. 277, 10244-10250
53. Tournier, C. et al. (2000) Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway. Science 288, 870-874
54. Behrens, A. et al. (1999) Amino-terminal phosphorylation of c-Jun regulates stress-induced apoptosis and cellular proliferation. Nat. Genet. 21, 326-329
55. Faris, M. et al. (1998) Stress-induced Fas ligand expression in T cells is mediated through a MEK kinase 1-regulated response element in the Fas ligand promoter. Mol. Cell. Biol. 18, 5414-5424
56. Yamamoto, K. et al. (1999) BCL-2 is phosphorylated and inactivated by an ASK1/Jun N-terminal protein kinase pathway normally activated at G2/M. Mol. Cell. Biol. 19, 8469-8478
57. Andreka, P. et al. (2001) Cytoprotection by Jun kinase during nitric oxide-induced cardiac myocyte apoptosis. Circ. Res. 88, 305-312
58. Minamino, T. et al. (1999) MEKK1 suppresses oxidative stress-induced apoptosis of embryonic stem cell-derived cardiac myocytes. Proc. Natl. Acad. Sci. U. S. A. 96, 15127-15132
59. Deng, X. et al. (2001) Novel role for JNK as a stress-activated Bcl-2 kinase. J. Biol. Chem. 276, 23681-23688
60. De Windt, L.J. et al. (2000) Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo: an apoptosis-independent model of dilated heart failure. Circ. Res. 86, 255-263
61. Saito, S. et al. (2000) β-Adrenergic pathway induces apoptosis through calcineurin activation in cardiac myocytes. J. Biol. Chem. 275, 34528-34533
62. Lotem, J. et al. (1999) Suppression or induction of apoptosis by opposing pathways downstream from calcium-activated calcineurin. Proc. Natl. Acad. Sci. U. S. A. 96, 12016-12020
63. Eto, Y. et al. (2000) Calcineurin is activated in rat hearts with physiological left ventricular hypertrophy induced by voluntary exercise training. Circulation 101, 2134-2137