Mitochondria in apoptosis of ischemic heart

FEBS Letters

Borutaite, Vilmante¹  Brown, Guy C¹ 

[1] Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK

关键词: Apoptosis;    Heart ischemia;    Mitochondrion;    Cytochrome c;    ARC;    apoptosis repressor with caspase recruitment domain;    Apaf-1;    apoptotic protease-activating factor;    BH3;    Bcl-2 homolog domain-2;    ER;    endoplasmic reticulum;    MPT;    mitochondrial permeability transition;    TNFα;    tumor necrosis factor-α;    VDAC;    voltage-dependent anion channel;   

DOI  :  10.1016/S0014-5793(03)00278-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown