Toll样受体2、4与心肌缺血再灌注损伤研究进展  

Progress of Toll-like Receptor 2 and 4 in Myocardial Ischemia/reperfusion Injury

作　　者：谢雨君[1] 黄玮[1] 

机构地区：[1]重庆医科大学附属第一医院心血管内科,重庆400016

出　　处：《心血管病学进展》2013年第2期240-243,共4页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金项目资助(30971212)

摘　　要：随着经皮冠状动脉介入治疗在冠心病患者中应用逐渐增多,缺血再灌注损伤的免疫机制目前正受到重视。研究发现,固有免疫的成员之一Toll样受体(TLR),在心肌缺血再灌注损伤的炎症反应中起了重要作用。正常心肌细胞在经历缺血-再灌注后能合成及释放一些物质,如热休克蛋白,其能与循环中及心肌细胞上TLR结合,最终激活核转录因子等而产生炎症反应。研究表明,心肌梗死后的炎症能影响左室重塑,最终可促进心肌梗死后心力衰竭的发生,了解其炎症反应中的免疫机制可对心肌梗死后心衰的防治提供新的思路,现将对TLR-2、TLR-4在心肌缺血再灌注损伤中的作用做一综述。With the development of the percutaneous coronary interventions for coronary heart disease, the myocardial ischemia/reperfusion （I/R） injury becomes more common. As a member of innate immunity, Toll-like receptor （TLR） may play an important role in the inflammation after the I/R injury. After ischemia, the cardiomyocyte can release some substance, like heat shock protein, which can bind to TLR. Through several signal transduction pathways, nuclear factor KB can be activated, which lead to the production of proinflammation fac- tors. Coincidently, inflammation post-myocardial infarction is a key determinant of the left ventricular remodeling and heart failure. Here we will provided new insight into the signal pathway of the TLR in the I/R injury.

关 键 词：TOLL样受体 缺血再灌注损伤 免疫 

分 类 号：R541[医药卫生—心血管疾病]