Nuclear-encoded mitochondrial proteins and their role in cardioprotection

被引:63
作者
Boengler, Kerstin [1 ]
Heusch, Gerd [1 ]
Schulz, Rainer [2 ]
机构
[1] Univ Klinikum Essen, Zentrum Innere Med, Inst Pathophysiol, D-45122 Essen, Germany
[2] Univ Giessen, Inst Physiol, Giessen, Germany
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2011年 / 1813卷 / 07期
关键词
Mitochondria; Ischemia/reperfusion; Cardioprotection; Import; Connexin; 43; Protein kinases; PERMEABILITY TRANSITION PORE; GLYCOGEN-SYNTHASE KINASE-3-BETA; KINASE-C ISOFORMS; PKC-EPSILON; REPERFUSION INJURY; OXIDATIVE STRESS; CONNEXIN-43; PHOSPHORYLATION; CARDIOMYOCYTE MITOCHONDRIA; CYTOCHROME-OXIDASE; CARDIAC MYOCYTES;
D O I
10.1016/j.bbamcr.2011.01.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
During myocardial ischemia/reperfusion, mitochondria are both a source and a target of injury. In cardioprotective maneuvers such as ischemic and pharmacological pre- and postconditioning mitochondria have a decisive role. Since about 99% of the mitochondrial proteins are encoded in the nucleus, deleterious and protective mitochondrial effects most likely comprise the import of cytosolic proteins. The present review therefore discusses the role of mitochondria in myocardial ischemia/reperfusion injury and protection from it, focusing on some cytosolic proteins, which are translocated into mitochondria before, during, or following ischemia/reperfusion. Both morphological and functional alterations are discussed at the level of the heart, the cardiomyocyte and/or the mitochondrion itself. This article is part of a Special Issue entitled: Mitochondria and Card ioprotection. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:1286 / 1294
页数:9
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