首页 | 本学科首页   官方微博 | 高级检索  
     

心肌缺血后处理胞内信号转导研究进展
引用本文:徐宪连,张英杰. 心肌缺血后处理胞内信号转导研究进展[J]. 生命科学, 2008, 20(1): 116-119
作者姓名:徐宪连  张英杰
作者单位:辽宁医学院附属第一医院,锦州,121001;辽宁医学院附属第一医院,锦州,121001
摘    要:缺血后处理对心肌再灌注损伤的保护是多因素参与的复杂过程。后处理对心肌的保护除了通过减少活性氧类物质的产生、抑制线粒体内钙超载、减轻内皮功能失调等被动作用外,还可主动激活再灌注损伤补救激酶(reperfusion injury salvage kinase,RISK)途径及其他蛋白激酶而实现。本文将对心肌缺血后处理中RISK通路的研究进展作一综述。

关 键 词:缺血后处理  再灌注损伤补救激酶  信号转导
文章编号:1004-0374(2008)01-0116-04
收稿时间:2007-05-21
修稿时间:2007-10-22

Advancements of signal transduction in myocardial ischemic postconditioning
XU Xian-lian,ZHANG Ying-jie. Advancements of signal transduction in myocardial ischemic postconditioning[J]. Chinese Bulletin of Life Sciences, 2008, 20(1): 116-119
Authors:XU Xian-lian  ZHANG Ying-jie
Affiliation:(The First Afilliated Hospital, Liaoning Medical College, Jinzhou121001, China)
Abstract:Ischemic postconditioning (IPO), which can attenuate myocardial reperfusion injury, is a complex process involving multiple factors. Besides the reduction in generation of reactive oxygen species, calcium overload in mitochondrion, endothelial dysfunction and so on (this is considered a "passive process"), IPO can also be an "active process" by activating the reperfusion injury salvage kinase (RISK) pathway and other kinases. The text will review the RISK pathway in the IPO in myocardium.
Keywords:ischemic postconditioning   reperfusion injury salvage kinase   signal transduction
本文献已被 维普 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号