铁死亡参与急性肾损伤的新机制

New mechanism of ferroptosis involved in acute kidney injury

急性肾损伤(AKI)是一种常见而严重的临床肾脏综合征,由多种生理和病理因素引起,以急性短暂肾功能降低为主要病征。其发病率和死亡率较高,且临床有效治疗策略有限。越来越多证据表明,铁死亡作为一种由脂质过氧化引起的铁依赖性、非凋亡形式的调节性细胞死亡方式,以铁过载、活性氧积累和脂质过氧化为典型特征,在横纹肌溶解、脓毒症、缺血再灌注损伤以及使用肾脏毒性药物等多种因素引起的急性肾损伤中扮演重要作用。本文旨在对铁死亡的诱发和防御机制及其参与AKI的作用途径等方面进行归纳和延伸,为后续相关研究提供理论依据。

Acute kidney injury(AKI)is a common and severe clinical renal syndrome caused by various physiological and pathological factors,which is mainly characterized by acute transient renal function reduction.Its morbidity and mortality are high,and effective clinical treatment strategies are limited.There is increasing evidence that ferroptosis,as an iron-dependent and non-apoptotic regulated cell death caused by lipid peroxidation,is characterized by iron overload,reactive oxygen species accumulation and lipid peroxidation.It plays an important role in AKI caused by rhabdomyolysis,sepsis,ischemia reperfusion injury and the use of nephrotoxic drugs.This paper aims to summarize and extend the inducing mechanism and the defense mechanism of ferroptosis as well as its pathways involved in AKI,so as to provide a theoretical basis for subsequent relevant studies.