The mitochondrial permeability transition pore and cyclophilin D in cardioprotection

被引:99
|
作者
Di Lisa, Fabio [1 ,2 ]
Carpi, Andrea [3 ]
Giorgio, Valentina [1 ,2 ]
Bernardi, Paolo [1 ,2 ]
机构
[1] Univ Padua, Dept Biomed Sci, I-35121 Padua, Italy
[2] Univ Padua, CNR, Inst Neurosci, I-35121 Padua, Italy
[3] European Inst Oncol, I-20139 Milan, Italy
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2011年 / 1813卷 / 07期
关键词
Mitochondria; Heart; Permeability transition; Cyclophilin D; Cardioprotection; CYCLOSPORINE-A-BINDING; REPERFUSION INJURY; CYTOCHROME-C; CELL-DEATH; CALCINEURIN; PROTECTION; HEART; ISOMERASE; TRANSLOCATION; INHIBITION;
D O I
10.1016/j.bbamcr.2011.01.031
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 play a central role in heart energy metabolism and Ca2+ homeostasis and are involved in the pathogenesis of many forms of heart disease. The body of knowledge on mitochondrial pathophysiology in living cells and organs is increasing, and so is the interest in mitochondria as potential targets for cardioprotection. This critical review will focus on the permeability transition pore (PTP) and its regulation by cyclophilin (CyP) D as effectors of endogenous protective mechanisms and as potential drug targets. The complexity of the regulatory interactions underlying control of mitochondrial function in vivo is beginning to emerge, and although apparently contradictory findings still exist we believe that the network of regulatory protein interactions involving the PTP and CyPs in physiology and pathology will increase our repertoire for therapeutic interventions in heart disease. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:1316 / 1322
页数:7
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