Research progress on the role of ferroptosis in the pathogenesis of abdominal aortic aneurysm
10.3760/cma.j.cn112434-20240626-00165
- VernacularTitle:铁死亡在腹主动脉瘤发生机制中的研究进展
- Author:
Zhuo LIU
1
;
Hongbo CI
Author Information
1. 新疆医科大学研究生院，乌鲁木齐 830000
- Publication Type:Journal Article
- From:
Chinese Journal of Thoracic and Cardiovascular Surgery
2025;41(1):59-62
- CountryChina
- Language:Chinese
-
Abstract:
Abdominal aortic aneurysm(AAA) is a severe disease characterized by the localized dilation of the abdominal aorta, with an increasing global incidence and a high mortality rate once the aneurysm ruptures. The pathogenesis of AAA is complex, and current non-surgical treatments have limited efficacy, necessitating the exploration of new therapeutic targets. Ferroptosis is a form of programmed cell death that relies on iron and is non-apoptotic, primarily characterized by the uncontrolled peroxidation of lipids in the cell membrane. Studies have found that ferroptosis is significantly upregulated in AAA through differential gene expression analysis of AAA tissues, predominantly occurring in vascular smooth muscle cells(VSMCs). Ferroptosis accelerates the progression of AAA by promoting phenotypic switching and cell death of VSMCs and inducing vascular calcification. Additionally, ferroptosis exacerbates AAA by increasing reactive oxygen species production, altering the intracellular oxidative stress balance, and inducing inflammatory responses. Inhibiting ferroptosis-related pathways, such as by overexpressing glutathione peroxidase 4(GPX4) or using ferroptosis inhibitors, has been shown to effectively slow the progression of AAA in mice. This review summarizes the mechanisms by which ferroptosis contributes to AAA progression and its potential therapeutic targets, aiming to provide new insights for the prevention and treatment of AAA.
