心肌缺血/再灌注损伤会破坏线粒体稳态平衡引起功能紊乱,如线粒体ATP合成减少、ROS生成增加、Ca^2+超载、膜通透性增加、线粒体片段化等,这些事件相互作用从多条途径参与I/R过程,是心肌I/R损伤的重要原因。对I/R中线粒体病理变化及I/R损伤线粒体保护途径的最新研究进展进行综述,为基于线粒体途径的心血管疾病药物防治研究提供参考。
Myocardial ischaemia/reperfusion (I/R) cause a wide array of alterations of mitochondrial homeostasis, such as loss of ATP synthesis, increase of ROS generation, Ca^2 + overload, membrane permeabilization, fragmentation of mitochondria and so on. The series of events are linked together and involved in the process of I/R injury, play critical roles in cardiomyocytes injury. This paper reviews the advancement of mitochondrial pathological changes during I/R and mitochondrial protective pathway of I/R injury, in order to understand the important mechanisms of I/R injury associated with mitochondria and pro- vide references for cardiovascular disease treatment strategies and drug development based on mitochondrial protection.