2014Molecular Cardiology of ChinaRequires access

Roles of Mitochondrial Permeability Transition Pore in Myocardial Ischemia/reperfusion Injury

LI Don

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Abstract

Mitochondria are pivotal organelles of cell metabolism, and mediating cardiomyocyte apoptosis induced by ischemia(hypoxia). The mitochondrial permeability transition pore(mPTP) is a large nonselective conductance pore located in the inner membrane of mitochondria, and it plays a crucial role for calcium homeostasis and cardiomyocyte injury. The irreversible opening of the mPTP may induce many harmful events, including mitochondrial structural damage, the decrease of mitochondrial membrane potential(ΔΨm) and apoptosis protein release. Delaying the opening of the mPTP upon reperfusion has been a potential target to reduce myocardial injury. The present article reviews the progress of components, mechanisms and the inhibitors of mPTP.

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Mitochondria are pivotal organelles of cell metabolism, and mediating cardiomyocyte apoptosis induced by ischemia(hypoxia). The mitochondrial permeability transition pore(mPTP) is a large nonselective conductance pore located in the inner membrane of mitochondria, and it plays a crucial role for calcium homeostasis and cardiomyocyte injury. The irreversible opening of the mPTP may induce many harmful events, including mitochondrial structural damage, the decrease of mitochondrial membrane potential(ΔΨm) and apoptosis protein release. Delaying the opening of the mPTP upon reperfusion has been a potential target to reduce myocardial injury. The present article reviews the progress of components, mechanisms and the inhibitors of mPTP.

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Available abstract

Mitochondria are pivotal organelles of cell metabolism, and mediating cardiomyocyte apoptosis induced by ischemia(hypoxia). The mitochondrial permeability transition pore(mPTP) is a large nonselective conductance pore located in the inner membrane of mitochondria, and it plays a crucial role for calcium homeostasis and cardiomyocyte injury. The irreversible opening of the mPTP may induce many harmful events, including mitochondrial structural damage, the decrease of mitochondrial membrane potential(ΔΨm) and apoptosis protein release. Delaying the opening of the mPTP upon reperfusion has been a potential target to reduce myocardial injury. The present article reviews the progress of components, mechanisms and the inhibitors of mPTP.

Key concepts: Mitochondrial permeability transition pore, MPTP, Mitochondrion, Mitochondrial membrane transport protein, Cell biology, Apoptosis, Membrane potential, Inner mitochondrial membrane

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