文献类型：期刊文献

英文题名：Molecular mechanisms of EPAS1 in regulating pulmonary vascular remodeling in COPD: a review

作者：Wang, Yunchao[1];Wang, Xinhua[2];Zhang, Yi[2];Lin, Lin[2];Ma, Xiaoming[3];Zheng, Guisen[1,2]

第一作者：Wang, Yunchao

通信作者：Zheng, GS[1];Zheng, GS[2];Ma, XM[3]

机构：[1]Gansu Univ Chinese Med, Inst Basic Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Inst Publ Hlth, Lanzhou 730000, Gansu, Peoples R China;[3]Lanzhou Pulm Hosp, Lanzhou 730000, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Inst Basic Med, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Inst Publ Hlth, Lanzhou 730000, Gansu, Peoples R China;[3]corresponding author), Lanzhou Pulm Hosp, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2026

卷号：53

期号：1

外文期刊名：MOLECULAR BIOLOGY REPORTS

收录：;Scopus(收录号：2-s2.0-105043720509);WOS:【SCI-EXPANDED(收录号:WOS:001811809000009)】；

基金：This study was supported by the following grants: 2022 Gansu Province Higher Education Institutions Industry Support Program Project No.2022CYZC-53 (Xinhua Wang); Gansu Provincial Science and Technology Programme 23JRRA1520 (Xinhua Wang); Lanzhou City Plan Project 2023-XD-151(Xiaoming Ma).

语种：英文

外文关键词：COPD; EPAS1; Vascular remodeling; MAPK signaling pathway; VEGF

摘要：Chronic obstructive pulmonary disease (COPD) is an incompletely reversible heterogeneous lung disease with high morbidity and mortality. Progressive worsening of dyspnea is its core clinical manifestation, and patients often develop severe complications such as pulmonary hypertension during the advanced stages of the disease. The oxygen-sensitive gene endothelial PAS domain-containing protein 1 (EPAS1) is a core transcription factor activated under hypoxic conditions. EPAS1 acts as a key regulator of hypoxia-induced pulmonary vascular remodeling in COPD, although other hypoxia-responsive factors, including HIF-1 alpha and NF-kappa B, also contribute to this complex process. This gene is involved in the pathological progression of COPD and is closely associated with pulmonary vascular remodeling. Pulmonary vascular remodeling, in turn, is a critical process in COPD pathogenesis, driven by chronic hypoxia, inflammatory responses, tobacco exposure, and cytokine dysregulation. These pathological changes can directly lead to the development of pulmonary hypertension and further exacerbate dyspnea symptoms. Under hypoxic conditions, aberrant expression of EPAS1 regulates the transcriptional activation of its target gene, vascular endothelial growth factor (VEGF), while also mediating the activation of the mitogen-activated protein kinase (MAPK) signaling pathway. These molecular events are closely related to the structural remodeling of pulmonary vasculature in COPD patients. Therefore, in-depth investigation into the molecular mechanisms by which EPAS1 regulates pulmonary vascular remodeling in the hypoxic microenvironment will not only help elucidate the pathogenesis of complications in advanced COPD but also provide potential molecular targets for clinical intervention, offering significant theoretical and clinical value for the precision treatment of COPD.