Mitochondrial calcium handling during ischemia-induced cell death in neurons

被引：67

作者：

Gouriou, Yves ^{[1
]}

Demaurex, Nicolas ^{[1
]}

Bijlenga, Philippe ^{[2
]}

De Marchi, Umberto ^{[1
]}

机构：

[1] Univ Geneva, Dept Cell Physiol & Metab, CH-1211 Geneva, Switzerland

[2] Univ Geneva, Dept Clin Neurosci & Dermatol, CH-1211 Geneva, Switzerland

来源：

BIOCHIMIE | 2011年 / 93卷 / 12期

关键词：

Calcium signaling; Brain diseases; Cerebral ischemia; Apoptosis; Bioenergetics; PERMEABILITY TRANSITION PORE; WOLF-HIRSCHHORN-SYNDROME; GLOBAL BRAIN ISCHEMIA; CYCLOSPORINE-A; CYCLOPHILIN-D; BENZODIAZEPINE-RECEPTOR; REPERFUSION INJURY; POTASSIUM CHANNEL; OXIDATIVE STRESS; POSTISCHEMIC REPERFUSION;

D O I：

10.1016/j.biochi.2011.08.001

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：

Mitochondria sense and shape cytosolic Ca2+ signals by taking up and subsequently releasing Ca2+ ions during physiological and pathological Ca2+ elevations. Sustained elevations in the mitochondrial matrix Ca2+ concentration are increasingly recognized as a defining feature of the intracellular cascade of lethal events that occur in neurons during cerebral ischemia. Here, we review the recently identified transport proteins that mediate the fluxes of Ca2+ across mitochondria and discuss the implication of the permeability transition pore in decoding the abnormally sustained mitochondrial Ca2+ elevations that occur during cerebral ischemia. (C) 2011 Elsevier Masson SAS. All rights reserved.

引用

页码：2060 / 2067

页数：8

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