The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection

被引：374
作者：
Bernardi, Paolo [1 ,2 ]
Di Lisa, Fabio [1 ,2 ]
机构：
[1] Univ Padua, Dept Biomed Sci, I-35121 Padua, Italy
[2] Univ Padua, CNR, Inst Neurosci, I-35121 Padua, Italy
来源：
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2015年 / 78卷
关键词：
Mitochondria; Permeability transition pore; Ischemia-reperfusion injury; PERIPHERAL BENZODIAZEPINE-RECEPTOR; CA-2&-INDUCED MEMBRANE TRANSITION; ISCHEMIA-REPERFUSION INJURY; ADRENAL-CORTEX MITOCHONDRIA; DEPENDENT ANION CHANNEL; MYOCARDIAL INFARCT SIZE; MALIC ENZYME-ACTIVITY; CYCLOPHILIN-D; ATP SYNTHASE; CYCLOSPORINE-A;
D O I：
10.1016/j.yjmcc.2014.09.023
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
The mitochondrial permeability transition (PT) - an abrupt increase permeability of the inner membrane to solutes - is a causative event in ischemia-reperfusion injury of the heart, and the focus of intense research in cardioprotection. The PT is due to opening of the PT pore (PIP), a high conductance channel that is critically regulated by a variety of pathophysiological effectors. Very recent work indicates that the PTP forms from the FATP synthase, which would switch from an energy-conserving to an energy-dissipating device. This review provides an update on the current debate on how this transition is achieved, and on the PTP as a target for therapeutic intervention. This article is part of a Special Issue entitled "Mitochondria: from basic mitochondrial biology to cardiovascular disease". (C) 2014 The Authors. Published by Elsevier Ltd.
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收藏
页码：100 / 106
页数：7
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