Mitochondria in Postconditioning

被引：52

作者：

Boengler, Kerstin ^{[1
]}

Heusch, Gerd ^{[1
]}

Schulz, Rainer ^{[1
]}

机构：

[1] Univ Klinikum Essen, Zentrum Innere Med, Inst Pathophysiol, D-45122 Essen, Germany

来源：

ANTIOXIDANTS & REDOX SIGNALING | 2011年 / 14卷 / 05期

关键词：

PERMEABILITY TRANSITION PORE; ISCHEMIA-REPERFUSION INJURY; K-ATP CHANNELS; GLYCOGEN-SYNTHASE KINASE-3-BETA; MYOCARDIAL INFARCT SIZE; BRIEF RENAL ISCHEMIA; ISOLATED RAT HEARTS; REACTIVE OXYGEN; FREE-RADICALS; SIGNALING PATHWAYS;

D O I：

10.1089/ars.2010.3309

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：

Several signal transduction pathways are activated by cardioprotective stimuli, including ischemic or pharmacological postconditioning. These pathways converge on a common target, the mitochondria, and cardioprotection by postconditioning is associated with preserved mitochondrial function after ischemia/reperfusion. The present review discusses the role of mitochondria in cardioprotection, especially the involvement of ATP-dependent potassium channels, reactive oxygen species, and the mitochondrial permeability transition pore, and focuses on the effects of postconditioning on mitochondrial function (i.e., their oxygen consumption and calcium retention capacity). The contribution of mitochondria to loss of protection by postconditioning in diseased or aged myocardium is also addressed. Antioxid. Redox Signal. 14, 863-880.

引用

页码：863 / U1

页数：19

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