ATP敏感性钾通道及其心肌保护作用机制的研究进展

Research progress of mitochondrial ATP-sensitive potassium channels in myocardial protection

背景心肌缺血／再灌注损伤（myocardial ischemia／reperfusion injury，MI／RI）引起严重的后果。虽然，缺血或药物预处理、缺血或药物后处理等处理方法均能达到心肌保护的作用，但是其心肌保护机制有待深入研究。目的总结ATP敏感性钾通道（ATP-sensitive potassium channel，KATP）及其心肌保护作用机制的研究进展。内容各种心肌保护方法能够直接开放KATP通道或通过激活G蛋白耦联受体间接开放KATP通道。与此同时，开放的KATP通道能够于再灌注早期刺激产生活性氧物质（reactiveoxygenspecies，ROS）及关闭线粒体通透性转换孔（mitochondrial permeability transition pore, mPTP）等方式减轻MI／RI。趋向各种心肌保护方法需要广泛应用于实践，包括KATP在内的各种机制需要更深入地研究。

Background Myocardial ischemia/reperfusion injury （MI/RI） can cause serious consequences. Preconditioning and posteonditioning can alleviate MI/RI, but their myocardial protective mechanisms need to be further explored. Objective To summarize the research progress of ATP-sensitive potassium channel（KATP） in myocardial protection. Content A lot of methods can open the KAw directly or indirectly by active the G protein-coupled receptors, and then, the opened KATe generate the reactive oxygen species （ROS） during the early period of reperfusion and close the mitochondrial permeability transition pores （mPTP） to alleviate MI/RI. Trend The methods and mechanisms of myocardial protection including KATe need to be further studied.