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Received:June 26, 2025 Published Online:May 01, 2026
Received:June 26, 2025 Published Online:May 01, 2026
中文摘要: 动脉粥样硬化(AS)是一种慢性炎性血管病变,以大中动脉管壁内斑块进行性积聚为特征。此过程涉及内皮细胞、平滑肌细胞及巨噬细胞的损害,它们在AS起始、进展及斑块易损性增加中起关键作用。 自噬、焦亡及铁死亡等细胞死亡机制在揭示AS的分子机制中具有重要意义,且这些机制在形态学、生物化学及遗传学上与其他细胞死亡模式显著不同。本综述综合当前研究进展,剖析这些细胞死亡机制间的相互作用,如何共同影响AS的病理进程及斑块稳定性,以期为AS的机制及治疗提供新见解。
Abstract:Atherosclerosis(AS)is a chronic inflammatory vascular disease characterized by progressive plaque accumulation in the walls of large and medium-sized arteries. This process involves damage to endothelial cells,smooth muscle cells and macrophages, which play key roles in the initiation and progression of AS as well as the increase in plaque vulnerability. Cell death mechanisms such as autophagy,pyroptosis and ferroptosis are important in revealing the molecular mechanisms of AS, and these mechanisms are significantly different from other cell death modes in morphology,biochemistry and genetics. This review summarizes the current research progress to analyze the crosstalk between these cell death mechanisms, in particular how they collectively affect the pathological course of AS and plaque stability. It is expected to provide new insights into the mechanism and treatment of AS.
文章编号: 中图分类号:R543.5 文献标志码:A
基金项目:陕西省自然科学基础研究一般项目(2024JC-YMBS-607);省级中医药中青年科技骨干人才项目(2023-ZQNY-015);陕西中医药大学非直属附属医院项目(2023FS02)
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