The cardiac mitochondrion: nexus of stress

Abstract

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.