Mechanisms of Cell Death in Heart Disease

被引:441
作者
Konstantinidis, Klitos [1 ,2 ,3 ]
Whelan, Russell S. [1 ,2 ,3 ]
Kitsis, Richard N. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA
[2] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10461 USA
[3] Albert Einstein Coll Med, Wilf Family Cardiovasc Res Inst, Bronx, NY 10461 USA
[4] Albert Einstein Coll Med, Diabet Res Ctr, Bronx, NY 10461 USA
[5] Albert Einstein Coll Med, Albert Einstein Canc Ctr, Bronx, NY 10461 USA
基金
美国国家卫生研究院;
关键词
apoptosis; cell death; heart failure; myocardial infarction; necrosis; MITOCHONDRIAL PERMEABILITY TRANSITION; CASPASE RECRUITMENT DOMAIN; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; ENDOPLASMIC-RETICULUM STRESS; CARDIAC MYOCYTE APOPTOSIS; CYCLOPHILIN-D; REPERFUSION INJURY; STRUCTURAL BASIS; INFARCT SIZE; CARDIOMYOCYTE APOPTOSIS;
D O I
10.1161/ATVBAHA.111.224915
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
The major cardiac syndromes, myocardial infarction and heart failure, are responsible for a large portion of deaths worldwide. Genetic and pharmacological manipulations indicate that cell death is an important component in the pathogenesis of both diseases. Cells die primarily by apoptosis or necrosis, and autophagy has been associated with cell death. Apoptosis has long been recognized as a highly regulated process. Recent data indicate that a significant subset of necrotic deaths is also programmed. In the review, we discuss the molecular mechanisms that underlie these forms of cell death and their interconnections. The possibility is raised that small molecules aimed at inhibiting cell death may provide novel therapies for these common and lethal heart syndromes. (Arterioscler Thromb Vasc Biol. 2012;32:1552-1562)
引用
收藏
页码:1552 / 1562
页数:11
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