NLRP3炎症小体介导氧化三甲胺加速动脉粥样硬化的新进展  

NLRP3 Inflammasome in Mediating Trimethylamine Oxide Accelerates Atherosclerosis

作　　者：赵海燕 关秀茹[1] ZHAO Haiyan;GUAN Xiuru(Department of Laboratory Diagnostics,The First Affiliated Hospital of Harbin Medical University,Harbin 150001,Heilongjiang,China)

机构地区：[1]哈尔滨医科大学附属第一医院检验科,黑龙江哈尔滨150001

出　　处：《心血管病学进展》2023年第11期1028-1032,共5页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金(81672084)。

摘　　要：动脉粥样硬化是一种伴有脂质代谢紊乱的慢性炎症反应。NOD样受体蛋白3(NLRP3)炎症小体作为一种多蛋白组成的炎症复合物,与细胞活性、血管炎症、斑块进展密切相关。氧化三甲胺作为肠道菌群主要代谢产物,能启动NLRP3炎症小体的激活,参与粥样硬化斑块形成和斑块破裂的病理学过程。现就氧化三甲胺与NLRP3炎症小体在动脉粥样硬化中的作用进行综述,旨在为动脉粥样硬化的机制研究和临床防治提供新视角。Atherosclerosis is a chronic inflammatory response with lipid metabolism disorder.NOD-like receptor protein 3(NLRP3)inflammasome,as a multi-protein inflammatory complex,is closely related to cell activity,vascular inflammatory,and the progression of plaque.Trimethylamine oxide,as a major metabolite of intestinal flora,can initiate the activation of NLRP3 inflammasome and participate in the pathophysiological mechanism of atherosclerotic plaque formation and plaque rupture.The paper reviews the role of NLRP3 inflammasome and trimethylamine oxide in atherosclerosis to provide a new perspective for the mechanism research and clinical prevention and treatment of atherosclerosis.

关 键 词：动脉粥样硬化 NOD样受体蛋白3炎症小体 氧化三甲胺 斑块破裂 

分 类 号：R543.5[医药卫生—心血管疾病]