自噬与内质网应激的相互关系及其在动脉粥样硬化发展和防治中的作用
姚树桐, 秦树存
泰山医学院动脉粥样硬化研究所,山东省高校动脉粥样硬化重点实验室;基础医学院,泰安 271000
摘要
自噬是细胞将受损蛋白质及细胞器运输至溶酶体进行消化降解的过程,是细胞维持内环境稳定的重要防御机制之一。近年来研究表明自噬在动脉粥样硬化病变中活性增强并参与其发病过程。氧化脂质、细胞因子及晚期糖基化终产物均可激活自噬,后者在动脉粥样硬化进展过程中发挥着保护或损伤性作用。然而自噬在动脉粥样硬化发展的不同阶段确切的作用及机制尚未完全阐明。本文总结了近年来有关血管细胞中的自噬反应及其在动脉粥样硬化发展中的作用研究进展,并讨论了自噬与内质网应激之间的相互关系以及自噬是否可作为动脉粥样硬化防治的新靶点。
关键词: 自噬; 动脉粥样硬化 ; 内质网应激 ; 治疗靶点
分类号:R363;R332
The relationship of autophagy with endoplasmic reticulum stress and its role in pathogenesis, prevention and therapy of atherosclerosis
YAO Shu-Tong, QIN Shu-Cun
Institute of Atherosclerosis, Key Laboratory of Atherosclerosis in Universities of Shandong; College of Basic Medical Sciences, Taishan Medical University, Taian 271000, China
Abstract
Autophagy is a cellular catabolic process responsible for removing the injured proteins and organelles via lysosome-dependent pathway, and it plays an important role in maintaining cellular homeostasis. Recent studies have shown that autophagy is activated and implicated in the pathogenesis of atherosclerosis. Autophagy can be triggered by oxidative lipids, cytokines and advanced glycation end products, and exerts protective or detrimental functions in the progression of atherosclerosis. However, the precise role and mechanisms of autophagy in different stages of atherosclerosis are still not fully clarified. This review highlights recent findings regarding autophagy response in vascular cells and its potential contribution to atherogenesis. Additionally, the relationship of autophagy with endoplasmic reticulum stress and whether autophagy could be a new therapeutic target for atherosclerosis are also discussed.
Key words: autophagy; atherosclerosis ; endoplasmic reticulum stress ; therapeutic target
收稿日期:2016-12-20 录用日期:2017-02-22
通讯作者:姚树桐,秦树存 E-mail: yst228@126.com, shucunqin@hotmail.com
引用本文:
姚树桐, 秦树存. 自噬与内质网应激的相互关系及其在动脉粥样硬化发展和防治中的作用[J]. 生理学报 2017; 69 (4): 515-521.
YAO Shu-Tong, QIN Shu-Cun. The relationship of autophagy with endoplasmic reticulum stress and its role in pathogenesis, prevention and therapy of atherosclerosis. Acta Physiol Sin 2017; 69 (4): 515-521 (in Chinese with English abstract).