© 1997 American Heart Association, Inc.
Articles |
Death by Design
Programmed Cell Death in Cardiovascular Biology and Disease
From the Molecular Cardiology Unit (W.R.M., M.D.S.), the Departments of Medicine (W.R.M.), Cell Biology (M.D.S.), and Molecular Physiology & Biophysics (M.D.S.), and Houston Veterans Affairs Medical Center (W.R.M.), Baylor College of Medicine, Houston, Tex.
Correspondence to Michael D. Schneider, MD, Molecular Cardiology Unit, Baylor College of Medicine, One Baylor Plaza, Room 506C, Houston, TX 77030. E-mail michaels{at}bcm.tmc.edu
Abstract Programmed cell death (apoptosis) is recognized, increasingly, as a contributing cause of cardiac myocyte loss with ischemia/reperfusion injury, myocardial infarction, and long-standing heart failure. Although the exact mechanisms initiating apoptosis in these in vivo settings remain unproven, insights into the molecular circuitry controlling apoptosis more widely suggest the potential to protect mammalian ventricular muscle from apoptosis through one or more of these pathways, by pharmacological means or, conceivably, gene transfer.
Key Words: apoptosis • gene transfer • heart failure • ischemia
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D. Zechner, R. Craig, D. S. Hanford, P. M. McDonough, R. A. Sabbadini, and C. C. Glembotski MKK6 Activates Myocardial Cell NF-kappa B and Inhibits Apoptosis in a p38 Mitogen-activated Protein Kinase-dependent Manner J. Biol. Chem., April 3, 1998; 273(14): 8232 - 8239. [Abstract] [Full Text] [PDF]
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Y. Wang, B. Su, V. P. Sah, J. H. Brown, J. Han, and K. R. Chien Cardiac Hypertrophy Induced by Mitogen-activated Protein Kinase Kinase 7, a Specific Activator for c-Jun NH2-terminal Kinase in Ventricular Muscle Cells J. Biol. Chem., March 6, 1998; 273(10): 5423 - 5426. [Abstract] [Full Text] [PDF]
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Y. Wang, S. Huang, V. P. Sah, J. Ross Jr., J. H. Brown, J. Han, and K. R. Chien Cardiac Muscle Cell Hypertrophy and Apoptosis Induced by Distinct Members of the p38 Mitogen-activated Protein Kinase Family J. Biol. Chem., January 23, 1998; 273(4): 2161 - 2168. [Abstract] [Full Text] [PDF]
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W. Wu, W.-L. Lee, Y. Y. Wu, D. Chen, T.-J. Liu, A. Jang, P. M. Sharma, and P. H. Wang Expression of Constitutively Active Phosphatidylinositol 3-Kinase Inhibits Activation of Caspase 3 and Apoptosis of Cardiac Muscle Cells J. Biol. Chem., December 15, 2000; 275(51): 40113 - 40119. [Abstract] [Full Text] [PDF]
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V. L. Gabai, A. B. Meriin, J. A. Yaglom, J. Y. Wei, D. D. Mosser, and M. Y. Sherman Suppression of Stress Kinase JNK Is Involved in HSP72-mediated Protection of Myogenic Cells from Transient Energy Deprivation. HSP72 ALLEVIATES THE STRESS-INDUCED INHIBITION OF JNK DEPHOSPHORYLATION J. Biol. Chem., November 22, 2000; 275(48): 38088 - 38094. [Abstract] [Full Text] [PDF]
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