E3泛素连接酶在缺血再灌注损伤中的机制和治疗潜力  

Mechanism and therapeutic potential of E3 ubiquitin ligase in ischemia-reperfusion injury

作　　者：曹楚仪 张进祥[1] CAO Chuyi;ZHANG Jinxiang(Department of Trauma Surgery,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Hubei Province,Wuhan 430022,China)

机构地区：[1]华中科技大学同济医学院附属协和医院创伤外科,湖北武汉430022

出　　处：《中国医药导报》2025年第9期55-59,共5页China Medical Herald

基　　金：国家自然科学基金资助项目(82170642)。

摘　　要：随着器官移植需求和技术发展,缺血再灌注成为影响患者术后恢复的主要并发症。E3泛素连接酶作为泛素化修饰的关键酶,通过调控蛋白质稳定性、功能及相互作用,参与缺血再灌注损伤的病理生理过程。本文综述E3泛素连接酶在缺血再灌注损伤中的最新研究进展,探讨其在细胞凋亡、线粒体功能、炎症反应及免疫调节中的作用机制,并评估其作为治疗靶点的潜力与挑战。With the demand for organ transplantation and technological development,ischemia-reperfusion has become the main complication affecting patients’postoperative recovery.E3 ubiquitin ligase,as a key enzyme for ubiquitination modification,participates in pathophysiological process of ischemia-reperfusion injury by regulating protein stability,function,and interactions.This article reviews the latest research progress of E3 ubiquitin ligase in ischemia-reperfusion injury,explores its action mechanism of cell apoptosis,mitochondrial function,inflammatory reaction,and immune regulation,and evaluates its potential and challenges as a therapeutic target.

关 键 词：缺血再灌注损伤 E3泛素连接酶 泛素化修饰 细胞凋亡 炎症反应 

分 类 号：R65[医药卫生—外科学]