自噬在动脉粥样硬化中的作用及其调控

自噬是一种通过溶酶体系统降解长半衰期蛋白和细胞器的过程.大量证据提示,进展型动脉粥样硬化斑块中存在着自噬现象.在离体实验中,利用一些能导致动脉粥样硬化形成的刺激物处理血管平滑肌细胞、巨噬细胞和内皮细胞,这些细胞均呈现一些自噬的特点,如髓鞘样结构、细胞质中泛素化包涵体聚集以及空泡形成增多.然而,尽管对自噬的研究兴趣不断增加,但对其在动脉粥样硬化中的确切作用还不清楚.因此,了解自噬的潜在细胞和分子机制,将为研究动脉粥样硬化性疾病的机制和治疗提供一条新的思路.

Role of autophgy in atherosclerosis and its modulation

Autophagy is a process for the degradation of long half-life proteins and organelles via the lysosome system. A large body of evidence indicates that the autophagic phenomena exist in the progressive atherosclerotic plaques. Vascular smooth muscle cells, macrophages, and endothelial cells treated with some stimulants that result in atherosclerosis formation in in vitro experiments, these cells show certain autophagic features, such as myelin-like structures, accumulation of ubiquitinated inclusions in the cytoplasm, and extensive vacuolization. However, although the interests in research on autophagy are increasing, the exact role of autophagy in atherosclerosis remains unclear. Therefore, understanding the underlying cellular and molecular mechanisms of autophagy will provide a new idea for studying the mechanisms and treatment of atherosclerotic disease.