The cardiac mitochondrion: nexus of stress.
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.
Baines
Christopher P
CP
The Dalton Cardiovascular Research Center, Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA. bainesc@missouri.edu
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D051017:Apoptosis Regulatory Proteins / Q000502:physiology; D006801:Humans; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D010539:Permeability; D018272:Porins / Q000502:physiology; D015221:Potassium Channels / Q000378:metabolism / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D013312:Stress, Physiological / Q000502:physiology*
D051017:Apoptosis Regulatory Proteins; D018272:Porins; D015221:Potassium Channels