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Mitochondrial calcium handling during ischemia-induced cell death in neurons

Published in Biochimie. 2011, vol. 93, no. 12, p. 2060-7
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.
Keywords AnimalsBrain Ischemia/metabolism/pathology/physiopathologyCalcium/metabolismCalcium-Binding ProteinsCell DeathCell HypoxiaHumansMitochondria/metabolismMitochondrial Membrane Transport Proteins/metabolismNeurons/metabolism/pathology
PMID: 21846486
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Research group Signaux intracellulaires (210)
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GOURIOU, Yves et al. Mitochondrial calcium handling during ischemia-induced cell death in neurons. In: Biochimie, 2011, vol. 93, n° 12, p. 2060-7. https://archive-ouverte.unige.ch/unige:21568

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Deposited on : 2012-06-13

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