铁稳态失调与急性肾损伤

Iron dyshomeostasis and acute kidney injury

铁是自然界所有生命的基本元素之一.由于游离铁可以提供单电子,并产生活性氧,因此它可能是生物系统中最强的氧化剂.铁介导的细胞损伤或铁死亡在急性肾损伤(AKI)的发病机制中起着十分重要的作用.机体中有多种既发挥铁的生物学作用,又可避免铁死亡的铁稳态调节蛋白和通路.铁调素通过调节介导铁输出的膜铁转运蛋白1(FPN1),可调节细胞内H-铁蛋白的表达水平,是迄今为止被人们所认识的机体铁稳态的关键调控因子.靶向调控铁调素、H-铁蛋白和FPN1表达,抑制铁死亡,可能是防治AKI的新思路、新策略.本文就铁稳态调节及其在AKI中的重要作用做一综述.

Iron is one of the primary essential elements for all life in nature.However,by the virtue of its ability to donate electrons,and generate reactive oxygen species,iron is probably the most effective oxidant in biologic systems.Iron-mediated cell injury or ferroptosis plays a crucial role in the pathogenesis of acute kidney injury(AKI).There are a variety of iron homeostasis regulatory proteins and pathways to allow the biological functions of iron yet avoid ferroptosis.Hepcidin serves as the key regulator of iron homeostasis through its ability to regulate ferroportin 1-mediated iron export and intracellular H-ferritin levels.Methods targeting hepcidin,H-ferritin,and feiToptosis-inhibiting pathways maybe offer exciting novel prospects and strategies to prevent or treat AKI.In this review we discuss iron homeostasis and highlight its importance in AKI.