Dai Jinjin, Chen Hongyang, Fang Jindong, Wu Shiguo, Jia Zhuangzhuang
School of Basic Medical Sciences, Yunnan University of Chinese Medicine, Kunming 650500, China.
Yunnan Key Laboratory of Integrated Traditional Chinese and Western Medicine for Chronic Disease in Prevention and Treatment, Kunming 650500, China.
Int J Mol Sci. 2025 Apr 30;26(9):4265. doi: 10.3390/ijms26094265.
Pulmonary hypertension (PH) is a serious cardiovascular disease caused by a variety of pathogenic factors, which is characterized by increased pulmonary vascular resistance (PVR) and progressive elevation of mean pulmonary artery pressure (mPAP). This disease can lead to right ventricular hypertrophy and, in severe cases, right heart failure and even death. Vascular remodeling-a pathological modification involving aberrant vasoconstriction, cell proliferation, apoptosis resistance, and inflammation in the pulmonary vascular system-is a significant pathological hallmark of PH and a critical process in its progression. Recent studies have found that vascular remodeling involves the participation of a diversity of cellular pathological alterations, such as the dysfunction of pulmonary artery endothelial cells (PAECs), the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs), the phenotypic differentiation of pulmonary artery fibroblasts, the inflammatory response of immune cells, and pericyte proliferation. This review focuses on the mechanisms and the intercellular crosstalk of these cells in the PH process, emphasizing recent advances in knowledge regarding cellular signaling pathways, inflammatory responses, apoptosis, and proliferation. To develop better treatments, a list of possible therapeutic approaches meant to slow down certain biological functions is provided, with the aim of providing new insights into the treatment of PH by simplifying the intricacies of these complex connections. In this review, comprehensive academic databases such as PubMed, Embase, Web of Science, and Google Scholar were systematically searched to discuss studies relevant to human and animal PH, with a focus on vascular remodeling in PH.
肺动脉高压（PH）是一种由多种致病因素引起的严重心血管疾病，其特征是肺血管阻力（PVR）增加和平均肺动脉压（mPAP）逐渐升高。这种疾病可导致右心室肥厚，严重时可导致右心衰竭甚至死亡。血管重塑——一种涉及肺血管系统异常血管收缩、细胞增殖、抗凋亡和炎症的病理改变——是PH的一个重要病理标志，也是其进展中的关键过程。最近的研究发现，血管重塑涉及多种细胞病理改变的参与，如肺动脉内皮细胞（PAECs）功能障碍、肺动脉平滑肌细胞（PASMCs）增殖和迁移、肺动脉成纤维细胞表型分化、免疫细胞炎症反应以及周细胞增殖。本综述重点关注这些细胞在PH过程中的机制和细胞间相互作用，强调细胞信号通路、炎症反应、凋亡和增殖方面的最新知识进展。为了开发更好的治疗方法，提供了一系列旨在减缓某些生物学功能的可能治疗方法，目的是通过简化这些复杂联系的复杂性，为PH的治疗提供新的见解。在本综述中，系统检索了PubMed、Embase、Web of Science和Google Scholar等综合学术数据库，以讨论与人类和动物PH相关的研究，重点是PH中的血管重塑。
