细胞自噬与雷帕霉素靶蛋白抑制在动脉粥样硬化中的研究进展  

Research progress of autophagy and mammalian target of rapamycin inhibition in atherosclerosis

作　　者：于菲[1] 荆红运 丁玲 关秀茹[1] Yu Fei;Jing Hongyun;Ding Ling;Guan Xiuru(Department of Laboratory Diagnosis,the First Affiliated Hospital of Harbin Medical University,Harbin 150001,China)

机构地区：[1]哈尔滨医科大学附属第一医院检验科,150001

出　　处：《国际免疫学杂志》2018年第4期457-460,共4页International Journal of Immunology

基　　金：国家自然科学基金（81672084）

摘　　要：动脉粥样硬化是一种以大动脉中脂质和纤维素沉积为特征的渐进性疾病,其在发展中国家的发病率呈逐年上升的趋势,引起的急性心血管事件和许多慢性损伤也是全球范围内死亡率,致残率增加的主要原因之一.自噬是维持细胞稳态,抵抗外界刺激的自我修复途径.自噬诱导剂雷帕霉素及其衍生物可以通过抑制雷帕霉素靶蛋白,减缓动脉粥样硬化的发生发展.现将雷帕霉素及其衍生物介导的mTOR抑制与动脉粥样硬化的关系进行重点阐述. Atherosclerosis（AS）is a progressive disease characterized by lipid and fibrin deposition in the large arteries. The prevalence of atherosclerotic arterial disease is increasing in developing countries. Acute cardiovascular events and many chronic injuries caused by atherosclerosis are one of the leading causes of mor-tality and disability worldwide. Autophagy is a self-repair process. It maintains cell stability and resists external stimuli. Rapamycin and rapalogs,the autophagy inducers,can be valuable for preventing the progress of AS by inhibiting mammalian target of rapamycin（mTOR）. This review focused on the relationship of atherosclerosis and mTOR inhibition mediated by rapamycin and rapalogs.

关 键 词：动脉粥样硬化 细胞自噬 雷帕霉素 雷帕霉素靶蛋白 

分 类 号：R543.5[医药卫生—心血管疾病]