内皮-间充质转化在肺动脉高压发病机制中的研究进展  

Pathogenesis of endothelial-mesenchymal transition in pulmonary arterial hypertension

作　　者：张静静 王岗[1] 李满祥[2] ZHANG Jing-jing;WANG Gang;LI Man-xiang(Department of Emergency Medicine,The Second Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710004,China;Department of Respiratory and Critical Care Medicine,The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061,China)

机构地区：[1]西安交通大学第二附属医院急诊科,陕西西安710004 [2]西安交通大学第一附属医院呼吸与危重症医学科,陕西西安710061

出　　处：《中国病理生理杂志》2018年第9期1724-1728,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81770057)

摘　　要：Endothelial-mesenchymal transition(EndMT)is a biological process through which endothelial cells change their endothelial phenotype into a mesenchymal or myofibroblastic phenotype with the expression of mesenchymal markers such asα-smooth muscle actin(α-SMA)and vimentin.When the pulmonary vascular endothelial cells are exposed to hypoxia and inflammatory stimulation,vascular smooth muscle cells in the outer and middle membrane accumulate through EndMT process,leading to pulmonary vascular remodeling and pulmonary arterial hypertension(PAH).Transforming growth factorβ(TGF-β)/bone morphogentic protein(BMP)signaling pathways promote EndMT process by bone morphogentic protein receptor 2(BMPR2)gene mutation which up-regulates high mobility group protein A1(HMGA1)gene and contributes to protein expression such as Slug and Snail,thus resulting in PAH.In brief,TGF-β/BMP signaling pathways and related regulators play an important role in pulmonary vascular reconstruction and the formation of PAH.Endothelial-mesenchymal transition(EndMT)is a biological process through which endothelial cells change their endothelial phenotype into a mesenchymal or myofibroblastic phenotype with the expression of mesenchymal markers such asα-smooth muscle actin(α-SMA)and vimentin.When the pulmonary vascular endothelial cells are exposed to hypoxia and inflammatory stimulation,vascular smooth muscle cells in the outer and middle membrane accumulate through EndMT process,leading to pulmonary vascular remodeling and pulmonary arterial hypertension(PAH).Transforming growth factorβ(TGF-β)/bone morphogentic protein(BMP)signaling pathways promote EndMT process by bone morphogentic protein receptor 2(BMPR2)gene mutation which up-regulates high mobility group protein A1(HMGA1)gene and contributes to protein expression such as Slug and Snail,thus resulting in PAH.In brief,TGF-β/BMP signaling pathways and related regulators play an important role in pulmonary vascular reconstruction and the formation of PAH.

关 键 词：肺动脉高压 内皮-间充质转化 Α-平滑肌肌动蛋白 TGF-β/BMP信号通路 

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