Basic Research in Cardiology

, Volume 104, Issue 2, pp 181–188 | Cite as

The mitochondrial permeability transition pore and ischemia-reperfusion injury

  • Christopher P. Baines


Mitochondrial dysfunction is an underlying cause of ischemia-reperfusion injury. In particular, ischemic injury induces dramatic increases in mitochondrial permeability, thereby instigating a chain of events that leads to both apoptotic and necrotic cardiomyocyte death. The mitochondrial permeability transition (MPT) pore, a large, non-specific channel that spans the inner mitochondrial membrane, is known to mediate the lethal permeability changes that initiate mitochondrial-driven cardiomyocyte death. The purpose of this review is to focus on the role of the MPT pore in ischemia-reperfusion injury, the mechanisms involved, and, in particular, what we do and do not know regarding the pore’s molecular composition.


Ischemia-reperfusion Mitochondrial permeability transition Voltage-dependent anion channel Adenine nucleotide translocase Cyclophilin-D Bcl-2 proteins 



We apologize that due to space constraints we have not been able to cite every important study pertaining to this subject. Work in the author’s laboratory is supported by grants from the National Institutes of Health (HL094404 and HL092327) and by an American Heart Association Scientist Development Grant (0635134N).


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Copyright information

© Springer-Verlag 2009

Authors and Affiliations

  1. 1.Department of Biomedical Sciences, Dalton Cardiovascular Research CenterUniversity of Missouri-ColumbiaColumbiaUSA

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