Nod样受体蛋白3炎症小体与动脉粥样硬化关系的研究现状与进展  

Advance in the Study of Nod-like Receptor Protein-3 Inflammasome and Atherosclerosis

作　　者：贾乙[1] 周丽 李晓辉[1] 

机构地区：[1]中国人民解放军第三军医大学药学院药物研究所,重庆市400038

出　　处：《中国动脉硬化杂志》2014年第1期79-84,共6页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金(81102448)

摘　　要：动脉粥样硬化能导致多种威胁人类健康的严重心血管疾病。除高血脂等经典危险因素外,炎症免疫因素作为新的危险因素已得到研究者的共识。Nod样受体蛋白3(NLRP3)炎症小体是机体固有免疫系统的一员,能够活化Caspase-1进而产生并释放成熟的促炎因子白细胞介素1β和白细胞介素18,参与体内非感染性炎症反应。研究证实NLRP3炎症小体活性与动脉粥样硬化的病变显著相关,并发现了多条NLRP3炎症小体激活通道。本文拟对NLRP3炎症小体与动脉粥样硬化形成之间关系的研究进展作一综述,并对具有潜力的药物靶点进行阐述。Atherosclerosis causes severe cardiovascular diseases, and those diseases are the most serious threats to public health. Inflammation was generally considered as a novel risk factor of atherosclerosis besides some classic factors, such as hyperlipemia. The Nod-like receptor protein-3 （NLRP3） inflammasome is a large muhimeric danger-sensing plat- form, as one of innate immunity response, promotes the activation of Caspase-1 and mediates the mature of pro-inflammato- ry cytokines interleukin-1β （IL-1 f3） and IL-18. Evidences have been provided that NLRP3 inflammasome has a critical role in the development of atherosclerosis. Here we discuss the advance in the role of NLRP3 Inflammasome in atherogen- esis, and the potential targets of atherosclerosis according to NLRP3 inflammasome.

关 键 词：Nod样受体蛋白3炎症小体 动脉粥样硬化 发病机制 

分 类 号：R363[医药卫生—病理学]