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神经元缺血性细胞死亡过程中线粒体钙离子处理。

Mitochondrial calcium handling during ischemia-induced cell death in neurons.

机构信息

Department of Cell Physiology and Metabolism, University of Geneva, rue Michel-Servet 1, Genève, Switzerland.

出版信息

Biochimie. 2011 Dec;93(12):2060-7. doi: 10.1016/j.biochi.2011.08.001. Epub 2011 Aug 10.

DOI:10.1016/j.biochi.2011.08.001
PMID:21846486
Abstract

Mitochondria sense and shape cytosolic Ca(2+) signals by taking up and subsequently releasing Ca(2+) ions during physiological and pathological Ca(2+) elevations. Sustained elevations in the mitochondrial matrix Ca(2+) 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 Ca(2+) across mitochondria and discuss the implication of the permeability transition pore in decoding the abnormally sustained mitochondrial Ca(2+) elevations that occur during cerebral ischemia.

摘要

线粒体通过在生理和病理钙离子升高期间摄取和随后释放钙离子来感知和塑造细胞质钙离子信号。线粒体基质钙离子浓度的持续升高,越来越被认为是在脑缺血期间神经元中发生的致命事件的细胞内级联反应的一个决定性特征。在这里,我们回顾了最近发现的介导钙离子跨线粒体流动的转运蛋白,并讨论了通透性转换孔在解码脑缺血期间发生的异常持续线粒体钙离子升高中的作用。

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