The Dalton Cardiovascular Research Center, Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA.
Annu Rev Physiol. 2010;72:61-80. doi: 10.1146/annurev-physiol-021909-135929.
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.
线粒体作为心肌细胞存活和死亡的关键调节因子的出现，彻底改变了心脏生物学领域。事实上，现在人们已经认识到，线粒体功能障碍在多种心脏疾病的发病机制中起着关键作用。现在已经发现了一系列线粒体蛋白/复合物，从经典的凋亡蛋白如 Bcl2 和 Bax，到线粒体通透性转换孔，再到离子通道如线粒体 K(ATP)通道和连接蛋白-43，它们都被认为是心脏细胞死亡的关键调节因子。因此，本综述的目的是集中讨论这些线粒体介导的细胞死亡抑制剂，并探讨其影响心脏病理的特定机制。
