肺血管内皮功能障碍在肺动脉高压中的研究进展

吴 晖1, 李晓 平*2
1、青海大学临床医学院
2、青海大学附属医院

摘要


肺动脉高压(PH)是一种以肺血管阻力增加为特征的严重心肺疾病,其核心病理机制包括内皮功能障碍、肺动脉平滑肌细胞(PASMC)和内皮细胞(PAEC)异常增殖、血管收缩及原位血栓形成。根据2022年ESC/ERS指南,肺高压(PH)分为五大类。流行病学数据显示,PH的发病率和患病率因地区和人群差异较大,女性患病率显著高于男性,但其机制尚未完全阐明。当前PH靶向药物多以缓解症状为主,难以逆转肺血管重塑。近年来研究表明,肺内皮功能障碍在PH的发生和进展中起关键调节作用,涉及血管收缩、结构重塑和纤维化等多种分子机制。内皮细胞(EC)功能紊乱是PH早期和核心事件,BMPR2信号通路的异常、线粒体损伤、活性氧(ROS)过度产生及氧化应激等可加剧病理进程。综上,内皮功能障碍及其相关信号通路异常是PAH发病和进展的核心环节,深入理解其分子机制有助于为PH的早期诊断和靶向治疗提供理论基础和新思路。

关键词


肺动脉高压;内皮功能障碍

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参考


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