铁死亡与炎症性肠病的研究进展
Research progress of ferroptosis and inflammatory bowel disease
摘要
炎症性肠病（IBD）是一组慢性非特异性胃肠道炎症性疾病，其病因和发病机制可能与环境、基因易感性、肠道微生物群和免疫反应相关。铁死亡是近年来发现的一种铁依赖的脂质氢过氧化物累积所致的细胞死亡，受到包括谷胱甘肽（GSH）和谷胱甘肽过氧化物酶4（GPx4）的脂质修复系统的严密调控。研究表明，IBD患者受损的肠道可表现出铁沉积、GSH耗竭、GPx4失活和脂质过氧化（LPO）等铁死亡的基本特征。此外，操纵铁死亡的关键基因可以改变IBD的进展、严重程度甚至发病率。本文概述了铁死亡的基本机制，并就近年来铁死亡的相关信号通路在IBD中的研究展望予以综述，为未来临床IBD的治疗提供新方向。
Abstract
Inflammatory bowel disease (IBD) is a group of chronic non-specific inflammatory conditions of the gastrointestinal tract, whose pathogenic factors and pathogenesis may be related to the environmental, susceptibility gene, gut microbiota and immune response. Ferroptosis, a new cell death, is typically accompanied by iron accumulation and lipid peroxidation and is tightly regulated by a lipid repair system including glutathione (GSH) and glutathione peroxidase 4 (GPx4). Increasing studies have enlightened that the fundamental features of ferroptosis, including iron deposition, GSH exhaustion, GPx4 inactivation, and lipid peroxidation, are manifested in the injured gastrointestinal tract in IBD patients. Furthermore, manipulation of the critical ferroptotic genes could alter the progression, severity, or even morbidity of IBD. In this review, we summarize the basic mechanism of ferroptosis and review the research prospect of ferroptosis signal pathways in IBD in recent years, to provide a new direction for the treatment of IBD in the future.关键词
炎症性肠病/铁死亡/活性氧/脂质过氧化引用本文复制引用
蒲瑜, 张吉翔, 董卫国.铁死亡与炎症性肠病的研究进展[EB/OL].(2022-10-13)[2026-04-02].https://chinaxiv.org/abs/202210.00093.学科分类
医药卫生理论/基础医学/内科学
评论