摘要
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、Ca2+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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2012年第12期1633-1636,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金重点项目(No 30830118)
重大新药创制综合性中药新药研究开发技术平台(No 2009ZX09301-005-007)
