A CaPful of mechanisms regulating the mitochondrial permeability transition

Despite the lack of its molecular identification, the mitochondrial permeability transition pore (PTP) 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 PTP...

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Bibliographic Details
Published inJournal of molecular and cellular cardiology Vol. 46; no. 6; pp. 775 - 780
Main Authors Di Lisa, Fabio, Bernardi, Paolo
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.06.2009
Subjects
Animals
Calcium
Calcium - metabolism
Cardiovascular
Cell death
Cyclophilins - metabolism
Cyclosporine - metabolism
Humans
Hydrogen-Ion Concentration
Mitochondria
Mitochondria - metabolism
Mitochondrial Membrane Transport Proteins - metabolism
Mitochondrial Permeability Transition Pore
Models, Biological
Peptidyl-Prolyl Isomerase F
Permeability transition
Phosphate
Phosphates - metabolism
Phosphates - physiology
Reperfusion
Permeability transition
Mitochondria
Reperfusion
Calcium
Cell death
Phosphate
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Summary:Despite the lack of its molecular identification, the mitochondrial permeability transition pore (PTP) 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 PTP 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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2009.03.006