低氧诱导肺动脉高压肺血管内皮-间充质转化作用机制的研究进展  

Progress in mechanism of hypoxia-induced pulmonary vascular endothelial-mesenchymal transition in pulmonary arterial hypertension

作　　者：王玉香 马兰[1] WANG Yuxiang;MA Lan(Research Center for High Altitude Medicine,Qinghai University,Xining 810001,China)

机构地区：[1]青海大学高原医学研究中心,青海西宁810008

出　　处：《中国病理生理杂志》2025年第4期804-808,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.32060207);青海省科技厅资助项目(No.2021-ZJ-738);2022年青海省“昆仑英才·高端创新创业人才”计划项目。

摘　　要：低氧可引起肺血管持续性收缩和肺血管重构,进而引发肺动脉高压(pulmonary hypertension,PH),严重时可导致右心衰竭。内皮-间充质转化(endothelial-mesenchymal transition,EndMT)是内皮细胞功能和表型向间充质细胞转化的生物学过程,是肺血管重构的关键因素。研究表明,低氧可通过作用于炎症、转录因子、信号通路、环状RNA、微小RNA等机制诱导PH肺血管EndMT。本文综述了低氧诱导PH肺血管EndMT作用机制的相关研究,以期为抑制PH肺血管重塑提供参考。Hypoxia leads to persistent constriction and remodeling of pulmonary blood vessels,resulting in pulmonary hypertension(PH)and,in severe cases,right heart failure.Endothelial-mesenchymal transition(EndMT)is a biological process in which endothelial cells undergo functional and phenotypic transformation into mesenchymal cells,playing a critical role in pulmonary vascular remodeling.Recent studies have revealed that hypoxia promotes pulmonary vascular EndMT in PH through the mechanisms involving inflammation,transcription factors,signaling pathways,circular RNAs,and microRNAs.This article provides a review of recent research on the mechanisms of hypoxia-induced pulmonary vascular EndMT in PH,with the aim of offering insights for inhibiting pulmonary vascular remodeling in PH.

关 键 词：低氧 肺动脉高压 内皮-间充质转化 

分 类 号：R543.2[医药卫生—心血管疾病] R459.9[医药卫生—内科学] R363[医药卫生—临床医学]