期刊
ANNUAL REVIEW OF PHYSIOLOGY
卷 72, 期 -, 页码 61-80出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021909-135929
关键词
cardiac disease; mitochondria; apoptosis; Bcl2 proteins; mitochondrial permeability transition; mitochondrial potassium channels; uncoupling proteins
类别
资金
- National Institutes of Health [HL094404, HL092327]
- American Heart Association Scientist Development [0635134N]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL094404, R21HL092327] Funding Source: NIH RePORTER
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.
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