Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress

被引：2195

作者：

Tabas, Ira ^{[1
,2
,3
]}

Ron, David ^{[4
]}

机构：

[1] Columbia Univ, Dept Med, New York, NY 10032 USA

[2] Columbia Univ, Dept Anat & Cell Biol, New York, NY 10032 USA

[3] Columbia Univ, Dept Physiol & Cellular Biophys, New York, NY 10032 USA

[4] Univ Cambridge, Inst Metab Sci, Cambridge CB2 0QQ, England

来源：

NATURE CELL BIOLOGY | 2011年 / 13卷 / 03期

基金：

美国国家卫生研究院; 英国惠康基金;

关键词：

UNFOLDED PROTEIN RESPONSE; PLASMA-CELL DIFFERENTIATION; CALMODULIN KINASE-II; ER STRESS; TRANSCRIPTION FACTOR; HOMOLOGOUS PROTEIN; OXIDATIVE STRESS; CARDIAC DYSFUNCTION; CHEMICAL CHAPERONES; MEDIATED APOPTOSIS;

D O I：

10.1038/ncb0311-184

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The ability to respond to perturbations in endoplasmic reticulum (ER) function is a fundamentally important property of all cells, but ER stress can also lead to apoptosis. In settings of chronic ER stress, the associated apoptosis may contribute to pathophysiological processes involved in a number of prevalent diseases, including neurodegenerative diseases, diabetes, atherosclerosis and renal disease. The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress.

引用

收藏

页码：184 / 190

页数：7

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