Cyclophilin D and myocardial ischemia-reperfusion injury: A fresh perspective

被引：77

作者：

Alam, Muhammad Rizwan ^{[1
]}

Baetz, Delphine ^{[1
]}

Ovize, Michel ^{[1
,2
,3
]}

机构：

[1] Univ Lyon 1, INSERM, CarMeN Lab, U1060, F-69373 Lyon, France

[2] Hosp Civils Lyon, Hop Louis Pradel, Serv Explorat Fonctionnelles Cardiovasc, F-69394 Lyon, France

[3] CIC Lyon, F-69394 Lyon, France

来源：

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2015年 / 78卷

关键词：

Ischemia-reperfusion; Cyclophilin D; Mitochondrial permeability transition pore; Cell death; Necrosis; MITOCHONDRIAL PERMEABILITY TRANSITION; ADENINE-NUCLEOTIDE TRANSLOCASE; COMPRISE VDAC MOLECULES; CYCLOSPORINE-A; ATP SYNTHASE; CELL-DEATH; PHOSPHATE CARRIER; CANCER-CELLS; SIMULATED ISCHEMIA; REGULATED NECROSIS;

D O I：

10.1016/j.yjmcc.2014.09.026

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Reperfusion is characterized by a deregulation of ion homeostasis and generation of reactive oxygen species that enhance the ischemia-related tissue damage culminating in cell death. The mitochondrial permeability transition pore (mPTP) has been established as an important mediator of ischemia-reperfusion (IR)-induced necrotic cell death. Although a handful of proteins have been proposed to contribute in mPTP induction, cyclophilin D (CypD) remains its only bona fide regulatory component. In this review we summarize existing knowledge on the involvement of CypD in mPIP formation in general and its relevance to cardiac IR injury in specific. Moreover, we provide insights of recent advancements on additional functions of CypD depending on its interaction partners and post-translational modifications. Finally we emphasize the therapeutic strategies targeting CypD in myocardial IR injury. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease". (C) 2014 Published by Elsevier Ltd.

引用

页码：80 / 89

页数：10

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