Role of mitochondria in apoptosis

被引：129

作者：

Gulbins, E ^{[1
]}

Dreschers, S ^{[1
]}

Bock, J ^{[1
]}

机构：

[1] Univ Essen Gesamthsch, Dept Biol Mol, D-45122 Essen, Germany

来源：

EXPERIMENTAL PHYSIOLOGY | 2003年 / 88卷 / 01期

关键词：

D O I：

10.1113/eph8802503

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Apoptosis is an evolutionary-conserved physiological mechanism to remove cells from an organism. Cellular apoptosis is mediated via an intracellular signalling programme that involves a variety of signalling molecules and cellular organelles including caspases, sphingomyelinases, Bcl-2-like proteins and proteins to cleave the DNA and mitochondria. Mitochondria contain several pro-apoptotic molecules that activate cytosolic proteins to execute apoptosis, block anti-apoptotic proteins in the cytosol and directly cleave nuclear DNA. Mitochondria trap these pro-apoptotic proteins and physically separate pro-apoptotic proteins from their cytoplasmic targets. Apoptosis is then initiated by the release of mitochondrial pro-apoptotic proteins into the cytosol. This process seems to be regulated by Bcl-2-like proteins and several ion channels, in particular the permeability transition pore (PTP) that is activated by almost all pro-apoptotic stimuli.

引用

页码：85 / 90

页数：6

共 45 条

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