Redox regulation of cardiomyocyte survival and death.
In this review, attempts were made to establish the role of reactive oxygen species as signaling molecules that regulate cardiomyocyte life and death during ischemia and reperfusion. Ischemia/reperfusion is a classical example because partial or mild ischemia can lead to simultaneous execution and repair of the cardiomyocytes, which is disrupted during severe ischemia leading to cell necrosis because of the lack of ATP. Apoptosis and repair processes are mediated by adaptive response in which oxygen free radicals function as typical signaling molecules through the activation of receptor tyrosine kinases, protein kinase C, and mitogen-activated protein kinases, as well as induction of redox-sensitive transcription factors and genes.
Das
D K
DK
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT 06030-1110, USA. DDAS@NEURON.UCHC.EDU
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D006801:Humans; D015428:Myocardial Reperfusion Injury / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
D017382:Reactive Oxygen Species