畜牧兽医学报 ›› 2025, Vol. 56 ›› Issue (8): 3666-3677.doi: 10.11843/j.issn.0366-6964.2025.08.011

• 综述 • 上一篇    下一篇

铁死亡与炎症相关性研究进展

温雪(), 许琬雪, 付壹彤, 杨洁, 付红玉, 樊瑞锋*()   

  1. 山东农业大学动物医学学院,泰安 271018
  • 收稿日期:2024-07-26 出版日期:2025-08-23 发布日期:2025-08-28
  • 通讯作者: 樊瑞锋 E-mail:17860815321@163.com;fanruifeng@sdau.edu.cn
  • 作者简介:温雪(2000-),女,山东滨州人,硕士生,主要从事动物营养代谢病与中毒病研究,E-mail:17860815321@163.com
  • 基金资助:
    国家自然科学基金(32273088;31902330)

Research Progress on the Relationship between Ferroptosis and Inflammation

WEN Xue(), XU Wanxue, FU Yitong, YANG Jie, FU Hongyu, FAN Ruifeng*()   

  1. College of Veterinary Medicine, Shandong Agricultural University, Tai′an 271018, China
  • Received:2024-07-26 Online:2025-08-23 Published:2025-08-28
  • Contact: FAN Ruifeng E-mail:17860815321@163.com;fanruifeng@sdau.edu.cn

摘要:

铁死亡是一种由铁超载、脂质过氧化和质膜损伤所触发的程序性细胞死亡方式,与机体内铁稳态、氧化还原系统等生理过程密切相关。炎症是机体重要的生理过程,对各种损伤刺激引发的防御性反应至关重要。最新研究表明,铁死亡与炎症反应过程密切相关,二者并不是简单的单向关系。铁死亡可以通过释放损伤相关分子模式(damage-associated molecular patterns,DAMPs)、脂质氧化产物和趋化因子等分子促进炎症反应,而炎症反应过程中激活的炎症通路(如JAK/STAT、NF-κB、炎症小体、cGAS-STING和MAPK)和分泌的细胞因子(如TNF-α、IL-1β和IL-10等)可以触发细胞铁死亡。本文重点介绍了铁死亡的分子机制及炎症反应过程中激活的常见炎症通路和分泌的细胞因子,并详细分析了铁死亡与炎症反应的相互作用及调控机制,为炎症性疾病提供新的治疗策略。

关键词: 铁死亡, 炎症, 脂质过氧化, 炎症通路

Abstract:

Ferroptosis is a form of programmed cell death initiated by iron overload, lipid peroxidation and plasma membrane damage. It is intimately associated with physiological processes such as iron homeostasis and the redox system within the organism. Inflammation is an essential physiological mechanism within the organism, facilitating defensive responses to various injurious stimuli. Recent studies have demonstrated that ferroptosis is closely related to the inflammatory response process, and that these two processes are not merely unidirectional. The promotion of inflammation by ferroptosis is facilitated by the release of damage-associated molecular patterns (DAMPs), lipid oxidation products and chemokine pathways. Conversely, inflammatory pathways (JAK/STAT, NF-κB, inflammasome, cGAS-STING and MAPK) activated during inflammation and secreted cytokines (TNF-α, IL-1β and IL-10) can also trigger cellular ferroptosis. This article focuses on the molecular mechanisms of ferroptosis, the common inflammatory pathways activated during the inflammatory response and the secreted cytokines. The interactions between ferroptosis and inflammatory responses and the regulatory mechanisms are also analyzed in detail, which offers insights into the development of novel therapeutic strategies for inflammatory diseases.

Key words: ferroptosis, inflammation, lipid peroxidation, inflammatory pathways

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