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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。
Autophagy is the process by which cells transport damaged proteins and organelles to lysosomes for digestion and degradation, and is one of the important defense mechanisms for cells to maintain stable internal environment. In recent years, studies have shown that autophagy in atherosclerotic lesions increased activity and participate in the pathogenesis. Autophagy is activated by oxidized lipids, cytokines and advanced glycation end products, which play a protective or damaging role in the development of atherosclerosis. However, the exact role and mechanism of autophagy in the different stages of atherosclerosis have not yet been fully elucidated. This review summarizes recent advances in autophagic response in vascular cells and their role in the development of atherosclerosis and discusses the interrelationship between autophagy and endoplasmic reticulum stress and whether autophagy can act as an artery A new target of prevention and treatment of atherosclerosis.