Journal
ANNUAL REVIEW OF PHYSIOLOGY
Volume 72, Issue -, Pages 19-44Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.physiol.010908.163111
Keywords
apoptosis; necrosis; autophagy; autophagic cell death; myocardial ischemia/reperfusion; myocardial infarction; cardiac remodeling
Categories
Funding
- NIH [R01HL60665, P01HL078825, P60DK020541]
- New York State Stem Cell Initiative
- Dr. Gerald and Myra Dorros Chair in Cardiovascular Disease
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL078825, R01HL060665] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P60DK020541] Funding Source: NIH RePORTER
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Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.
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