Mitochondria in apoptosis of ischemic heart.
Apoptosis in the heart can be triggered by ischemia and/or reperfusion depending on conditions. This may involve activation of plasma membrane death receptors and/or translocation of Bcl-2 homologous proteins to mitochondria. However, one of the main mechanisms for triggering this apoptosis appears to be mitochondrial permeability transition followed by cytochrome c release. Cytochrome c release can result in caspase activation and thus apoptosis, but also results in mitochondrial dysfunction, which might contribute to contractile dysfunction or necrosis at reperfusion.
Borutaite
Vilmante
V
Department of Biochemistry, University of Cambridge, UK. vb207@mole.bio.cam.ac.uk
Brown
Guy C
GC
D017209:Apoptosis; D003574:Cytochrome c Group / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D008929:Mitochondria, Heart / Q000378:metabolism / Q000502:physiology*; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology
D003574:Cytochrome c Group; D007473:Ion Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore