铁死亡在溃疡性结肠炎中的研究进展  

Research Progress of Ferroptosis in Ulcerative Colitis

作　　者：陈琴 彭栎帆 徐瑞 娄龙 彭子运 CHEN Qin;PENG Lifan;XU Rui;LOU Long;PENG Ziyun(Department of Proctology,Kunming Municipal Hospital of Traditional Chinese Medicine,Kunming 650011,China)

机构地区：[1]昆明市中医医院肛肠科,昆明650011

出　　处：《中国医学科学院学报》2024年第4期619-624,共6页Acta Academiae Medicinae Sinicae

基　　金：云南省中医药应用基础研究联合专项-面上项目(202101AZ070001-268、202301AZ070001-089);昆明市卫生健康委员会卫生科研课题(2022-04-01-009);昆明市卫生科技人才培养项目暨“十百千”工程[2022-SW(后备)-60]。

摘　　要：溃疡性结肠炎(UC)是一种慢性炎症性肠病,特征为肠道黏膜的持续炎症和溃疡形成,其发病机制涉及免疫功能障碍、肠道微生物群失调和炎症所引起的黏膜损伤。铁死亡是一种铁依赖性细胞死亡形式,其调控机制包括铁代谢紊乱、脂质过氧化和谷胱甘肽(GSH)耗竭。已有研究表明,铁死亡在UC的发病过程中起关键作用,特别是在调节炎症反应和损伤肠道上皮细胞方面。本文综述了铁死亡的调控机制及其在UC中的作用,探讨了通过调节铁代谢、减少脂质过氧化和维护GSH水平来缓解UC症状的潜在治疗策略,为UC的诊断和治疗提供了新的靶点和方向。Ulcerative colitis(UC)is a chronic inflammatory bowel disease characterized by continuous inflammation and ulcer formation in the intestinal mucosa.Its pathogenesis involves immune dysfunction,dysbiosis of gut microbiota,and mucosal damage caused by inflammation.Ferroptosis is an iron-dependent form of cell death regulated by disturbances in iron metabolism,lipid peroxidation,and depletion of glutathione(GSH).Studies have indicated that ferroptosis plays a crucial role in the pathogenesis of UC,particularly in regulating inflammatory responses and damaging intestinal epithelial cells.This article reviews the regulatory mechanisms and roles of ferroptosis in UC and discusses the potential therapeutic strategies to alleviate UC symptoms by modulating iron metabolism,reducing lipid peroxidation,and maintaining GSH levels,providing new targets and directions for the diagnosis and treatment of UC.

关 键 词：溃疡性结肠炎 铁死亡 铁代谢紊乱 脂质过氧化 谷胱甘肽耗竭 

分 类 号：R574.1[医药卫生—消化系统]