title: Cyclophilin D and myocardial ischemia-reperfusion injury: a fresh perspective.
abstract: 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 mPTP 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".
authors.affiliation: INSERM U1060, CarMeN Laboratory, Claude Bernard Lyon 1 University, F-69373 Lyon, France.
authors.forename: Muhammad Rizwan
authors.initials: MR
authors.lastname: Alam
authors.affiliation: INSERM U1060, CarMeN Laboratory, Claude Bernard Lyon 1 University, F-69373 Lyon, France.
authors.forename: Delphine
authors.initials: D
authors.lastname: Baetz
authors.affiliation: INSERM U1060, CarMeN Laboratory, Claude Bernard Lyon 1 University, F-69373 Lyon, France; Hospices Civils de Lyon, Hôpital Louis Pradel, Service d'Explorations Fonctionnelles Cardiovasculaires & CIC de Lyon, F-69394 Lyon, France. Electronic address: michel.ovize@chu-lyon.fr.
authors.forename: Michel
authors.initials: M
authors.lastname: Ovize
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D016923:Cell Death; D000081406:Peptidyl-Prolyl Isomerase F; D021983:Cyclophilins / Q000378:metabolism*; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D011485:Protein Binding; D011499:Protein Processing, Post-Translational; D015398:Signal Transduction
chemical_list: D002352:Carrier Proteins; D000081406:Peptidyl-Prolyl Isomerase F; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D021983:Cyclophilins; D002118:Calcium
keywords: Cell death; Cyclophilin D; Ischemia–reperfusion; Mitochondrial permeability transition pore; Necrosis