Mitochondrial Permeability Transition Pore And Myocardial Ischemia-reperfusion Injury

Ischemia-reperfusion injury post myocardial infarction is a challengeand a hot topic in cardiovascular disease. The opening of themitochondrial permeability transition pore (mitochondrial permeabilitytransition pore, MPTP) is considered to be closely related to myocardialischemia-reperfusion injury, and it is a key effector. The constructure ofMPTP includes voltage dependent anion channel,adenine nucleotidetranslocator, cyclophilin D and other proteins. Under physiologicalconditions, MPTP is closed, only has selective permeability of somemitochondrial metabolic substrates and ion. In the ischemia-reperfusionprocess, due to a variety of triggers, MPTP can be opened by decrease ofintracellular cAMP, Ca2+overload, oxidative stress, Bcl-2family proteinsand other mechanisms, its open causes mitochondrial rupture, leading tothe release of pro-apoptotic substances that can initiate apoptosis.However, if the stress is severe or persistent, ATP required for startingapoptosis is depleted, then will cause cell necrosis. The inhibition of itsopening may have the effect of myocardial protection, ischemicpre-conditioning and ischemic post-conditioning are powerful myocardialprotection measures that can greatly improve injury due to acuteischemia and reperfusion. With the extensive application of genomics,there has been some new discoveries. This paper would make a review of the structure,function,mechanism of MPTP in ischemia-reperfusion injury.