Nakamura Kazufumi, Akagi Satoshi, Ejiri Kentaro, Taya Satoshi, Saito Yukihiro, Kuroda Kazuhiro, Takaya Yoichi, Toh Norihisa, Nakayama Rie, Katanosaka Yuki, Yuasa Shinsuke
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Center for Advanced Heart Failure, Okayama University Hospital, Okayama 700-8558, Japan.
Int J Mol Sci. 2025 Jan 20;26(2):835. doi: 10.3390/ijms26020835.
Pulmonary hypertension associated with lung diseases and/or hypoxia is classified as group 3 in the clinical classification of pulmonary hypertension. The efficacy of existing selective pulmonary vasodilators for group 3 pulmonary hypertension is still unknown, and it is currently associated with a poor prognosis. The mechanisms by which pulmonary hypertension occurs include hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, a decrease in pulmonary vascular beds, endothelial dysfunction, endothelial-to-mesenchymal transition, mitochondrial dysfunction, oxidative stress, hypoxia-inducible factors (HIFs), inflammation, microRNA, and genetic predisposition. Among these, hypoxic pulmonary vasoconstriction and subsequent pulmonary vascular remodeling are characteristic factors involving the pulmonary vasculature and are the focus of this review. Several factors have been reported to mediate vascular remodeling induced by hypoxic pulmonary vasoconstriction, such as HIF-1α and mechanosensors, including TRP channels. New therapies that target novel molecules, such as mechanoreceptors, to inhibit vascular remodeling are awaited.
与肺部疾病和/或缺氧相关的肺动脉高压在肺动脉高压临床分类中归为第3组。现有的选择性肺血管扩张剂对第3组肺动脉高压的疗效尚不清楚,目前其预后较差。肺动脉高压发生的机制包括低氧性肺血管收缩、肺血管重塑、肺血管床减少、内皮功能障碍、内皮-间充质转化、线粒体功能障碍、氧化应激、缺氧诱导因子(HIFs)、炎症、微小RNA以及遗传易感性。其中,低氧性肺血管收缩及随后的肺血管重塑是涉及肺血管系统的特征性因素,也是本综述的重点。据报道,有几个因素可介导低氧性肺血管收缩诱导的血管重塑,如HIF-1α和机械感受器,包括瞬时受体电位(TRP)通道。人们期待有针对新分子(如机械感受器)来抑制血管重塑的新疗法。