氧化应激下铁死亡及铁稳态调节IPF的研究进展  

Research progress on ferroptosis and iron homeostasis in regulating idiopathic pulmonary fibrosis under oxidative stress

作　　者：赵可 所鸿[2] Zhao Ke;Suo Hong(Graduate School of Inner Mongolia Medical University,Hohhot 010000,Inner Mongolia Autonomous Region,China;Department of Respiratory Medicine,The Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010000,Inner Mongolia Autonomous Region,China)

机构地区：[1]内蒙古医科大学研究生院,呼和浩特010000 [2]内蒙古医科大学附属医院呼吸科,呼和浩特010000

出　　处：《中国基层医药》2024年第11期1756-1760,共5页Chinese Journal of Primary Medicine and Pharmacy

摘　　要：特发性肺纤维化(IPF)是一种病因未明、机制复杂的疾病。近年来,铁死亡作为一种可调控的细胞死亡方式被发现。目前的研究表明,在氧化应激状态下,铁死亡及铁稳态的调节失衡与IPF的发生、发展密切相关。该文通过综述氧化应激状态下IPF的发生、发展以及在氧化应激调控下铁死亡、铁稳态失衡导致IPF的发生机制,为进一步探究IPF提供全新思路和潜在的治疗靶点。Idiopathic pulmonary fibrosis(IPF)is a disease of unknown etiology with a complex pathogenesis.In recent years,ferroptosis,a regulated form of cell death,has been identified as a significant factor in various diseases.Current research indicates that the imbalance in the regulation of ferroptosis and iron homeostasis under oxidative stress is closely related to the onset and progression of IPF.This article reviews the mechanisms by which oxidative stress contributes to the development of IPF,as well as how the dysregulation of ferroptosis and iron homeostasis under oxidative stress leads to the disease.Findings from this article provide new insights and potential therapeutic targets for further investigation of IPF.

关 键 词：特发性肺纤维化 氧化性应激 细胞死亡 铁 过氧化脂质类 综述 

分 类 号：R363[医药卫生—病理学]