基础医学与临床 ›› 2026, Vol. 46 ›› Issue (3): 440-444.doi: 10.16352/j.issn.1001-6325.2026.03.0440

• 短篇综述 • 上一篇    下一篇

铁死亡在急性心肌梗死后心室重构中的研究进展

古丽胡马·阿不都克然木, 迪丽达尔·希力甫, 阿迪拉·阿扎提*   

  1. 新疆医科大学第一附属医院 心血管内科,新疆 乌鲁木齐 830054
  • 收稿日期:2025-06-24 修回日期:2025-09-24 出版日期:2026-03-05 发布日期:2026-02-25
  • 通讯作者: *adlndl@163.com
  • 基金资助:
    新疆维吾尔自治区科技厅上合国际项目(2022E01037)

Progress of ferroptosis in ventricular remodeling after acute myocardial infarction

Gulihuma·ABUDUKERANMU, Dilidaer·XILIFU, Adila·AZHATI*   

  1. Department of Cardiology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China
  • Received:2025-06-24 Revised:2025-09-24 Online:2026-03-05 Published:2026-02-25
  • Contact: *adlndl@163.com

摘要: 铁死亡是一种新型铁依赖性细胞死亡方式,近年来在急性心肌梗死(AMI)后心室重构中的作用备受关注。研究发现,AMI后心肌缺血、缺氧、铁超载及氧化应激可激活铁死亡通路,通过谷胱甘肽过氧化物酶4(GPX4)失活、脂质活性氧(ROS)累积等机制,导致心肌细胞死亡和间质纤维化,从而促进心室重构的发生。动物模型证实,铁死亡抑制剂可减轻心肌损伤并改善心室重塑。综上,抑制铁死亡有望成为未来防治AMI后心室重构的新的治疗思路。

关键词: 铁死亡, 心肌梗死, 心室重塑, 心力衰竭

Abstract: Ferroptosis is a new type of iron-dependent cell death, and its role in ventricular remodeling after acute myocardial infarction has attracted much attention in recent years. Studies have found that myocardial ischemia,hypoxia, iron overload and oxidative stress after AMI can activate the ferroptosis pathway, leading to cardiomyocyte death and interstitial fibrosis through mechanisms such as glutathione peroxidase 4 (GPX4) inactivation and lipid reactive oxygen species (ROS) accumulation, thereby promoting ventricular remodeling. Researches with animal models have confirmed that ferroptosis inhibitors or iron chelators can reduce myocardial injury and improve ventricular remodeling. In summary, inhibition of ferroptosis is expected to become a new strategy for the prevention and treatment of ventricular remodeling after AMI in the future.

Key words: ferroptosis, myocardial infarction, ventricular remodeling, heart failure

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