AI Article Synopsis
- Autophagy is a crucial cellular process that removes damaged proteins and organelles and helps maintain cell health, particularly in the context of atherosclerosis.
- Recent research indicates that autophagy can be activated by factors like oxidative lipids and cytokines, and it may have both protective and harmful effects on the progression of atherosclerosis.
- The review explores how autophagy is linked to vascular cells, its relationship with endoplasmic reticulum stress, and the possibility of targeting autophagy for new atherosclerosis therapies.
Article 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.
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