线粒体通透性转换孔
线粒体
程序性细胞死亡
细胞生物学
生物
连接蛋白
线粒体膜转运蛋白
细胞凋亡
心肌细胞
DNAJA3公司
心肌细胞
线粒体内膜
未折叠蛋白反应
线粒体融合
心肌细胞
神经科学
线粒体DNA
内质网
细胞内
缝隙连接
生物化学
基因
标识
DOI:10.1146/annurev-physiol-021909-135929
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.
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