Borutaite Vilmante, Brown Guy C
Department of Biochemistry, University of Cambridge, UK.
FEBS Lett. 2003 Apr 24;541(1-3):1-5. doi: 10.1016/s0014-5793(03)00278-3.
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.
心脏中的细胞凋亡可根据具体情况由缺血和/或再灌注触发。这可能涉及质膜死亡受体的激活和/或Bcl-2同源蛋白向线粒体的转位。然而,触发这种细胞凋亡的主要机制之一似乎是线粒体通透性转换,随后是细胞色素c的释放。细胞色素c的释放可导致半胱天冬酶激活,从而引发细胞凋亡,但也会导致线粒体功能障碍,这可能导致再灌注时的收缩功能障碍或坏死。