NLRP3炎性体在胰岛素致动脉粥样硬化中的作用机制  

Pathogenesis of NLRP3 Inflammasome in Insulin Induced Atherosclerosis

作　　者：刘念[1] 王旭开[1] 

机构地区：[1]第三军医大学大坪医院心血管内科,重庆400042

出　　处：《心血管病学进展》2013年第1期75-78,共4页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金项目(81170281)

摘　　要：动脉粥样硬化与2型糖尿病关系密切,70%的2型糖尿病患者合并发生动脉粥样硬化。最近的观点将2型糖尿病和动脉粥样硬化都归为代谢综合征,具有全身性炎症的特点。在炎症中,一种被称为NLRP3炎性体的蛋白复合物对细胞因子白介素-1β有促进生成及成熟的作用。胆固醇结晶以及胰岛淀粉样多肽均可激活炎性体。炎症所导致的胰岛素抵抗和高胰岛素血症对大血管内皮及血管壁平滑肌亦有复杂的作用。Atherosclerosis is closely associated with type 2 diabetes mellitus, and 70% of type 2 diabetes patients develop atheroscle- rosis. Recent studies have classified both diseases as a metabolism syndrome that possess a characteristic of systemic inflammation. A protein complex known as inflammasome, which promotes inflammation via the secretion of IL-1β, links atherosclerosis with type 2 diabetes. The cholesterol crystals in atherosclerosis and islet amyloid polypeptide in type 2 diabetes are able to activate inflammasome. Inflammation in turn can cause insulin resistance, accompanyed by hyperinsulinemia, which has reticula effects on vascular endothelium cells and smooth muscle cells. This article examines the mechanism by which the inflammasome contributes to insulin induced atheroselerosis.

关 键 词：NLRP3炎性体 胰岛素 动脉粥样硬化 发病机制 

分 类 号：R587.1[医药卫生—内分泌] R543.5[医药卫生—内科学]