%0 Journal Article
%T 肾脏缺血再灌注损伤与铁死亡关系的研究进展<br>Research Progress on the Relationship between Kidney Ischemia-Reperfusion Injury and Ferroptosis
%A 樊清睿
%A 李荣
%A 梁学海
%A 高文胜
%A 雷小楠
%A 蒲含波
%A 杜春
%J Advances in Clinical Medicine
%P 227-239
%@ 2161-8720
%D 2024
%I Hans Publishing
%R 10.12677/acm.2024.1451418
%X 肾脏缺血再灌注损伤(Ischemia-Reperfusion Injury, IRI)是导致急性肾损伤(Acute kidney injury, AKI)，影响肾移植效果及心脏手术后肾功能恢复的关键因素。该过程由缺血阶段的氧气和营养物质供应不足以及随后再灌注阶段的氧化应激和炎症反应引发的细胞与组织损伤组成。铁死亡，一种与铁代谢紊乱有关的细胞死亡形式，其通过铁依赖性脂质过氧化导致细胞死亡，近年来，研究发现铁死亡在多种肾脏疾病的发病机制中扮演着重要角色，尤其是在肾脏IRI中。本综述旨在探讨肾脏IRI与铁死亡机制的联系，并总结当前通过抑制铁死亡对肾脏IRI治疗的研究进展，旨在为肾脏IRI的预防与治疗提供新的理论支撑。<br />
Kidney ischemia-reperfusion injury (IRI) is a key factor leading to acute kidney injury (AKI), affecting kidney transplant outcomes and post-cardiac surgery kidney function recovery. This process consists of cell and tissue damage triggered by the lack of oxygen and nutrient supply during the ischemic phase and oxidative stress and inflammatory responses during the subsequent reperfusion phase. Ferroptosis, a form of cell death associated with dysregulated iron metabolism that leads to cell death through iron-dependent lipid peroxidation, has recently been found to play a significant role in the pathogenesis of various kidney diseases, especially in kidney IRI. This review aims to explore the connection between kidney IRI and the mechanism of ferroptosis, and to summarize current research progress in treating kidney IRI by inhibiting ferroptosis, providing new theoretical support for the prevention and treatment of kidney IRI.
%K 肾脏缺血再灌注损伤，铁死亡，机制，信号通路，脂质过氧化，治疗<br>Kidney Ischemia-Reperfusion Injury
%K Ferroptosis
%K Mechanism
%K Signaling Pathway
%K Lipid Peroxidation
%K Treatment
%U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=86256