The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan City People’s Hospital, Qingyuan, Guangdong, China.
Department of Pathophysiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China.
Aging (Albany NY). 2020 Nov 4;12(21):22335-22349. doi: 10.18632/aging.103786.
The development of atherosclerosis is accompanied by the functional deterioration of plaque cells, which leads to the escalation of endothelial inflammation, abnormal vascular smooth muscle cell phenotype switching and the accumulation of lipid-laden macrophages within vascular walls. Autophagy, a highly conserved homeostatic mechanism, is critical for the delivery of cytoplasmic substrates to lysosomes for degradation. Moderate levels of autophagy prevent atherosclerosis by safeguarding plaque cells against apoptosis, preventing inflammation, and limiting the lipid burden, whereas excessive autophagy exacerbates cell damage and inflammation and thereby accelerates the formation of atherosclerotic plaques. Increasing lines of evidence suggest that long noncoding RNAs can be either beneficial or detrimental to atherosclerosis development by regulating the autophagy level. This review summarizes the research progress related to 1) the significant role of autophagy in atherosclerosis and 2) the effects of the lncRNA-mediated modulation of autophagy on the plaque cell fate, inflammation levels, proliferative capacity, and cholesterol metabolism and subsequently on atherogenesis.
动脉粥样硬化的发展伴随着斑块细胞功能恶化，导致内皮炎症加剧、血管平滑肌细胞表型异常转换以及富含脂质的巨噬细胞在血管壁内堆积。自噬是一种高度保守的稳态机制，对于将细胞质底物递送至溶酶体进行降解至关重要。适度的自噬通过保护斑块细胞免受细胞凋亡、抑制炎症和限制脂质负担来预防动脉粥样硬化，而过度的自噬会加剧细胞损伤和炎症，从而加速动脉粥样硬化斑块的形成。越来越多的证据表明，长非编码 RNA 可以通过调节自噬水平对动脉粥样硬化的发展产生有益或有害的影响。本文综述了自噬在动脉粥样硬化中的重要作用以及 lncRNA 介导的自噬调控对斑块细胞命运、炎症水平、增殖能力和胆固醇代谢的影响，进而对动脉粥样硬化发生的相关研究进展。
