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: Muhammad Rizwan Alam, Delphine Baetz, Michel Ovize
• Journal: Journal of molecular and cellular cardiology (J Mol Cell Cardiol) Vol. 78 Pg. 80-9 (Jan 2015) ISSN: 1095-8584 [Electronic] England
• PMID: 25281838 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2014. Published by Elsevier Ltd.

Chemical References

• Carrier Proteins
• Cyclophilin D
• Mitochondrial Membrane Transport Proteins
• Mitochondrial Permeability Transition Pore
• Cyclophilins
• Calcium

Topics

• Animals
• Calcium (metabolism)
• Carrier Proteins (metabolism)
• Cell Death
• Cyclophilin D
• Cyclophilins (metabolism)
• Humans
• Mitochondria, Heart (metabolism)
• Mitochondrial Membrane Transport Proteins (metabolism)
• Mitochondrial Permeability Transition Pore
• Myocardial Reperfusion Injury (metabolism)
• Protein Binding
• Protein Processing, Post-Translational
• Signal Transduction