CAJ | 학술논문

局部缺血部位快速再灌注虽然保护了心肌,但也引起再灌注损伤.目前还没有减轻再灌注损伤的特效疗法,但近年来研究显示,G蛋白耦联受体(G protein-coupled receptor,GPCR)的激动剂、胰岛素和缺血后处理可以在各种实验条件和各类动物模型中有效抵抗再灌注损伤.这些干预手段启动的心脏保护机制可能包括激活再灌注损伤补救激酶(reperfusion injury salvage kinase,RISK)途径、抑制糖原合酶激酶-3β(glycogen synthase kinase 3β,GSK-3β)以及抑制线粒体膜通透性转换孔(mitochondrial permeability transition pore,mPTP)开放等.这些研究成果有利于开发治疗急性心肌梗死的有效临床手段.
국부결혈부위쾌속재관주수연보호료심기,단야인기재관주손상.목전환몰유감경재관주손상적특효요법,단근년래연구현시,G단백우련수체(G protein-coupled receptor,GPCR)적격동제、이도소화결혈후처리가이재각충실험조건화각류동물모형중유효저항재관주손상.저사간예수단계동적심장보호궤제가능포괄격활재관주손상보구격매(reperfusion injury salvage kinase,RISK)도경、억제당원합매격매-3β(glycogen synthase kinase 3β,GSK-3β)이급억제선립체막통투성전환공(mitochondrial permeability transition pore,mPTP)개방등.저사연구성과유리우개발치료급성심기경사적유효림상수단.
Early restoration of blood flow to the ischemic myocardium not only saves myocardium but also induces reperfusion injury.While no specific therapy to reduce reperfusion injury has yet been established, recent laboratory studies have shown that G proteincoupled receptor (GPCR) agonists, insulin, and postconditioning can effectively prevent reperfusion injury in various experimental settings and animal species. The potential mechanisms underlying the cardioprotection initiated by these interventions may include activation of the reperfusion injury salvage kinase (RISK) pathway, inactivation of glycogen synthase kinase 3β (GSK-3β), and modulation of mitochondrial permeability transition pore (mPTP) opening. These encouraging laboratory findings may help us develop successful clinical strategies to salvage reperfused myocardium in patients with acute myocardial infarction.