A CaPful of mechanisms regulating the mitochondrial permeability transition

被引:106
作者
Di Lisa, Fabio
Bernardi, Paolo
机构
[1] Univ Padua, Dept Biomed Sci, I-35121 Padua, Italy
[2] Univ Padua, CNR, Inst Neurosci, I-35121 Padua, Italy
关键词
Permeability transition; Cell death; Calcium; Phosphate; Reperfusion; Mitochondria; MYOCARDIAL REPERFUSION INJURY; DEPENDENT CELL-DEATH; 2 SEPARATE SITES; CYCLOSPORINE-A; CYCLOPHILIN-D; ISCHEMIA-REPERFUSION; PYRIDINE-NUCLEOTIDES; CARDIAC ISCHEMIA; RECENT PROGRESS; HEART-FAILURE;
D O I
10.1016/j.yjmcc.2009.03.006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Despite the lack of its molecular identification, the mitochondrial permeability transition pore (FTP) is a fascinating subject because of its important role in cell death. This holds especially true for cardiovascular diseases and in particular for ischemia-reperfusion injury, where research on FFP inhibition has been successfully translated from bench to clinical evidence of cardioprotection. In addition, recent reports extend the relevance of PTP to heart failure and atherosclerosis. This review summarizes the major factors involved in PTP control with specific emphasis on cardiovascular pathophysiology, and highlights recent findings on the pivotal role of inorganic phosphate as a mediator of the inhibitory effects of cyclosporin A and cyclophilin D ablation. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:775 / 780
页数:6
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