线粒体通透性转换孔在缺血后处理中的作用和机制.pdf

oadingofcalciumionandopeningofmitochondrialpermeabilitytransitionpore(mPTP).Thusreperfusioncaninducemitochondrialswellingandouter—membranerupturingandleadtomyocardialcellnecrosis.mPTP,themitochondrialnonspecifictransitionpore,posedofvoltage—dependentanionchannel(VDAC),adeninenucleotidetranslocator(ANT)andcyclophilinD(CYPD).ClosedmPTPcanmaintaintheintegratedstructureofmitochondrial,whichiscritica1totheischemicmyocardialinfunctionrecovery.ThemechanismofischemicpostconditioninginprotectingthemyocardialcellisreducingROS,preventingtheoverloadingofcalciumion,releasingtheprotectiveendogenousmediator,activatingthereperfusioninjurysalvagekinase(RISK)andinhibitingtheopeningofmPTP.Keywordsreperfusioninjury;mitochondrialpermeabilitytransitionpore;ischemicpostcondicjoning;reperfusioninjurysalvagekinase