Mitochondria and ischemia–reperfusion injury of the heart: Fixing a hole

Ischemia and post-ischemic reperfusion cause a wide array of functional and structural alterations of mitochondria. Although mitochondrial impairment is recognized as pivotal in determining loss of viability, the causal relationships among the various processes involved is ill defined. Nevertheless,...

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Bibliographic Details
Published in:Cardiovascular research 2006-05, Vol.70 (2), p.191-199
Main Authors: Di Lisa, Fabio, Bernardi, Paolo
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Calcium - metabolism
Cardiology. Vascular system
Cell Death
Cyclophilins - metabolism
Humans
Ischemia
Ischemic Preconditioning, Myocardial
Medical sciences
Mitochondria
Mitochondria, Heart - metabolism
Mitochondria, Heart - pathology
Mitochondrial Membrane Transport Proteins - metabolism
Mitochondrial Permeability Transition Pore
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - pathology
Peptidyl-Prolyl Isomerase F
Permeability transition
Reactive oxygen species
Reactive Oxygen Species - metabolism
Signal Transduction - physiology
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Summary:Ischemia and post-ischemic reperfusion cause a wide array of functional and structural alterations of mitochondria. Although mitochondrial impairment is recognized as pivotal in determining loss of viability, the causal relationships among the various processes involved is ill defined. Nevertheless, a wide consensus exists in attributing a crucial role to opening of the mitochondrial permeability transition pore (PTP). Strong support for this concept has recently been provided by the reduced infarct size observed in mice lacking cyclophilin D. This protein located within the mitochondrial matrix favours PTP opening by increasing its sensitivity to Ca2+ in a process that is antagonized by cyclosporin A. Genetic approaches have also been used to demonstrate that adenine nucleotide translocase is not an essential component of the PTP. Here, we discuss our current understanding of the structure and function of PTP in the context of heart injury caused by ischemia and reperfusion.
ISSN:0008-6363
1755-3245
DOI:10.1016/j.cardiores.2006.01.016