摘要
缺血再灌注损伤(IRI)常继发于心肌梗死、缺血性卒中、急性肾损伤等病理过程,也可出现在临床治疗过程中,如溶栓治疗、经皮冠状动脉介入治疗、器官移植等.因此,如何针对IRI进行预防和治疗一直是临床上面临的难题.EP3 受体可通过氧化应激、炎症反应、细胞凋亡等多种途径来调控细胞功能,其在IRI中发挥着重要的作用.因此,EP3 受体可能成为IRI中新的治疗靶点.本文将从心肌IRI、脑IRI、缺血性肾损伤等角度,对EP3 受体在IRI中的作用及可能机制进行分析综述,以期为临床上治疗缺血再灌注损伤提供理论依据.
Abstract
Ischemia-reperfusion injury(IRI)is often secondary to pathological processes such as myocardial infarction,ischemic stroke and acute kidney injury,and can also appear in clinical treatment,such as thrombolytic therapy,percutaneous coronary intervention,organ transplantation,etc.Consequently,preventing and treating IRI remains a significant challenge in clinical practice.The EP3 receptor regulates cellular functions through various pathways,including oxidative stress,inflammatory responses and apoptosis,and it plays an important role in IRI.Thus,receptor EP3 may represent a promising new therapeutic target for IRI.This article analyzes and reviews the role and possible mechanisms of EP3 receptor in IRI from the perspectives of myocardial IRI,cerebral IRI and ischemic kidney injury,aiming to provide a theoretical basis for the clinical treatment of ischemia-reperfusion injury.
维普
万方数据