Apoptosis in heart and skeletal muscle.
Apoptosis, or programmed cell death, is now recognized to be an important cellular event during normal development and in the progression of specific diseases. Apoptosis can be triggered by stimuli initiating outside of the cell, or within the mitochondria, leading to the activation of caspases and subsequent cell death. Although apoptosis has been widely studied in a variety of tissues over the last 5 years, skeletal muscle and heart have been relatively ignored in this regard. Research on apoptosis in cardiac muscle has recently taken on a higher profile as the recognition emerges that it may be an important contributor to specific cardiac pathologies, particularly in response to ischemia-reperfusion in which reactive oxygen species are formed. In skeletal muscle, very few studies have been done under specific physiological (e.g., exercise) and pathophysiological (e.g., dystrophies, denervation, myopathies) conditions. Skeletal muscle is unique in that it is multi-nucleated, and evidence suggests that it can undergo individual myonuclear apoptosis as well as complete cell death. This review discusses the basic cellular mechanisms of apoptosis, as well as the current evidence of this process in cardiac and skeletal muscle. The need for more work in this area is highlighted, particularly in exercise and training.
Primeau
Andy J
AJ
School of Kinesiology and Health Science, York University, Toronto, Ontario, M3J 1P3.
Adhihetty
Peter J
PJ
Hood
David A
DA
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D020169:Caspases / Q000502:physiology; D015444:Exercise / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D020287:In Situ Nick-End Labeling; D019157:Ischemic Preconditioning, Myocardial; D008931:Mitochondria, Muscle / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000502:physiology*; D018482:Muscle, Skeletal / Q000166:cytology* / Q000502:physiology; D009136:Muscular Dystrophies / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D014157:Transcription Factors / Q000502:physiology
D017382:Reactive Oxygen Species; D014157:Transcription Factors; D020169:Caspases