低氧性肺动脉高压(hypoxic pulmonary hypertension,HPH)是慢性肺源性心脏病和各型高原病的关键病理生理变化,最终可致右心室衰竭,甚至死亡。其发病环节主要包括低氧性肺血管收缩和肺血管重塑。肺动脉平滑肌细胞(pulmonary arterial smooth muscle cells, PASMCs)是构成肺动脉壁的主要细胞,其增殖肥大是HPH 结构重塑的重要病理特征。因此,探究肺动脉平滑肌细胞的增殖状态是肺血管结构重塑的核心研究领域。葡萄糖-6-磷酸脱氢酶(glucose-6-phosphate dehydrogenase, G6PD)通路己经成为国内外研究的热点信号通路之一,抑制G6PD干预低氧性肺动脉高压中肺动脉平滑肌细胞重塑可以逆转HPH。为了更清晰理解HPH 发病机制与G6PD 通路之间的关系,本文围绕G6PD调控低氧诱导的PASMCs代谢转变与增殖的研究进展进行综述, 以期为临床治疗HPH 提供新的思路。

Hypoxic pulmonary hypertension (HPH) is a key pathophysiological change in chronic pulmonary heart disease and various types of high-altitude diseases,which can ultimately lead to right ventricular failure and even death.Its pathogenesis mainly includes hypoxic pulmonary vasoconstriction and pulmonary vascular remodeling.Pulmonary arterial smooth muscle cells (PASMCs) are the main arterial cells that constitute the pulmonary artery wall,and their hypertrophy and proliferation are significant pathological features of HPH structural remodeling. Therefore,exploring the proliferative status of PASMCs is a core research area in pulmonary vascular structural remodeling.The glucose - 6- phosphate dehydrogenase (G6PD) pathway has emerged as one prominent focus both domestically and internationally. Intervening in PASMCs remodeling in HPH by inhibiting G6PD can reverse HPH. To better understand the relationship between the pathogenesis of HPH and the G6PD pathway, this review focuses on the research progress concerning the role of G6PD in regulating hypoxia-induced metabolic shifts and proliferation in PASMCs. The aim is to provide novel perspectives for the clinical treatment of HPH.