Mitochondria in apoptosis of ischemic heart

Abstract

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.