氧化还原信号在心肌缺血再灌注损伤中保护作用机制的研究进展

被引：9

作者：

陈德 ^{[1
]}

滕爱兰 ^{[2
]}

周荣 ^{[1
]}

机构：

[1] 兰州大学第一医院

[2] 甘肃省第二人民医院

来源：

中国循环杂志 | 2013年 / 28卷 / 07期

关键词：

氧化还原信号; 心肌缺血; 再灌注; 保护;

D O I：

暂无

中图分类号：

R541 [心脏疾病];

学科分类号：

1002 ; 100201 ;

摘要：

心肌缺血再灌注会导致活性氧化物(Reactive oxygen species,ROS)的生成,减少有效一氧化氮(Nitric oxide,NO)浓度,导致钙离子(Ca2+)超载,线粒体通透性转换孔的长时间开放,并导致心肌梗死、心律不齐等。缺血再灌注损伤的有效防治一直是医学界高度重视的课题,缺血前预处理和缺血后处理是缺血再灌注损伤的有效防治手段。对再灌注损伤防治的联合保护信号转导通路已有大量研究,其中氧化还原机制在缺血再灌注过程中起到重要的作用。心脏保护的信号转导机制包括如由ROS诱导的氧化还原,NO及衍生物诱导的亚硝基化,硫化氢诱导的S基化,O-联糖基化等。具有心肌保护的信号通路主要集中在线粒体,而多种线粒体蛋白在预处理和后处理中成为翻译后修饰的靶点。所有这些机制可产生交互作用并影响和改变心肌缺血再灌注的损伤。

引用

页码：545 / 548

页数：4

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