《生命科学》 2017, 29(4): 353-363

内质网应激与自噬及其交互效应: 动脉粥样硬化潜在的治疗新靶标

田晋帆1， 刘　玥2*，李立志3*，吕树铮1

(1 首都医科大学附属北京安贞医院心血管科，北京 100029；2 中国中医科学院西苑医院
    心血管病中心，北京 100091；3 中国中医科学院心血管病研究所，北京 100091)

摘　要：摘　要：持续的内质网应激是导致细胞凋亡和继发的组织功能障碍的重要病理机制之一。在氧化应激、高同型半胱氨酸、高胆固醇水平及胰岛素抵抗等情况下，未折叠蛋白反应会被持续过度激活，促进动脉粥样硬化的发生发展。自噬是细胞自我更新，维持内环境稳态，同时调节营养代谢的重要方式之一。近年来研究表明，内质网应激、细胞自噬及其交互效应在动脉粥样硬化形成及发展中扮演了重要角色，内质网应激、细胞自噬及其交互作用是未来治疗动脉粥样硬化性疾病的新靶标。

Endoplasmic reticulum stress， autophagy and their crosstalk: the potential treatment targets for atherosclerosis

TIAN Jin-Fan1， LIU Yue2*， LI Li-Zhi3*， LV Shu-Zheng1

(1 Department of Cardiology， Beijing Anzhen Hospital of Capital Medical University， Beijing 100029， China; 2 Cardiovascular Disease Centre， Xiyuan Hospital of China Academy of Chinese Medical Sciences， Beijing 100091， China; 3 China Heart Institute of Chinese Medicine， China Academy of Chinese Medical Sciences， Beijing 100091， China)

Abstract: Abstract: Sustainable endoplasmic reticulum stress (ERS) is one of the major pathologic mechanisms for cell apoptosis and secondary tissue dysfunction. The unfolded protein response (UPR) will be sustainably over-activated in the case of oxidative stress， hyperhomocysteinemia， hypercholesterolemia and insulin resistance， thus promoting the occurrence and development of atherosclerosis. Autophagy is one of the important ways for cell self-renewal， maintaining homeostasis and regulating the metabolism of nutrients. In recent years， it has been demonstrated that ERS， auctophagy and the crosstalk between them play pivotal roles in the development of atherosclerosis. Consequently， they will be potential treatment targets for atherosclerosis.