The Cardiac Mitochondrion: Nexus of Stress

被引:121
作者
Baines, Christopher P. [1 ]
机构
[1] Univ Missouri, Dalton Cardiovasc Res Ctr, Dept Biomed Sci, Columbia, MO 65211 USA
基金
美国国家卫生研究院;
关键词
cardiac disease; mitochondria; apoptosis; Bcl2; proteins; mitochondrial permeability transition; mitochondrial potassium channels; uncoupling proteins; PERMEABILITY TRANSITION PORE; DEPENDENT ANION CHANNEL; SENSITIVE K+ CHANNEL; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; ADENINE-NUCLEOTIDE TRANSLOCASE; CASPASE RECRUITMENT DOMAIN; BCL-2; FAMILY-MEMBERS; PROTEIN-KINASE-C; CYCLOPHILIN-D; CELL-DEATH;
D O I
10.1146/annurev-physiol-021909-135929
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The emergence of mitochondria as critical regulators of cardiac myocyte survival and death has revolutionized the field of cardiac biology. Indeed, it is now well recognized that mitochondrial dysfunction plays a crucial role in the pathogenesis of multiple cardiac diseases. A panoply of mitochondrial proteins/complexes ranging from canonical apoptosis proteins such as Bcl2 and Bax, through the mitochondrial permeability transition pore, to ion channels such as mitochondrial K-ATP channels and connexin-43 have now been implicated as critical regulators of cardiac cell death. The purpose of this review, therefore, is to focus on these mitochondrial mediators/inhibitors of cell death and to address the specific mechanisms that underlie their ability to influence cardiac pathology.
引用
收藏
页码:61 / 80
页数:20
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