Mitochondria in apoptosis of ischemic heart

被引：120

作者：

Borutaite, V

Brown, GC

机构：

[1] Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England

[2] Kaunas Univ Med, Inst Biomed Res, Kaunas, Lithuania

来源：

FEBS LETTERS | 2003年 / 541卷 / 1-3期

关键词：

apoptosis; heart ischemia; mitochondrion; cytochrome C;

D O I：

10.1016/S0014-5793(03)00278-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

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页码：1 / 5

页数：5

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