The relationship of autophagy with endoplasmic reticulum stress and its role in pathogenesis, prevention and therapy of atherosclerosis.
- Author:
Shu-Tong YAO
1
;
Shu-Cun QIN
2
Author Information
1. Institute of Atherosclerosis, Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian 271000, China.
2. Institute of Atherosclerosis, Key Laboratory of Atherosclerosis in Universities of Shandong, Taishan Medical University, Taian 271000, China. shucunqin@hotmail.com.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2017;69(4):515-521
- CountryChina
- Language:Chinese
-
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.
