Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 78, Issue -, Pages 80-89Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2014.09.026
Keywords
Ischemia-reperfusion; Cyclophilin D; Mitochondrial permeability transition pore; Cell death; Necrosis
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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.
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