Ma Wende, Ma Yumei, Bai Yuting, Su Xiaoling
Qinghai University, Xining, Qinghai, China; Compact Medical Service Community in Menyuan County, Menyuan, Qinghai, China.
Department of Digestive, Qinghai Provincial People's Hospital, Xining, Qinghai, China.
Anatol J Cardiol. 2025 Mar 10;29(5):210-21. doi: 10.14744/AnatolJCardiol.2025.5013.
High-altitude pulmonary hypertension (HAPH) is a condition characterized by elevated pulmonary arterial pressure exceeding normal physiological values, resulting from a combination of high-altitude low-pressure, hypoxic environments, genetic susceptibility, immune dysfunction, and neurogenic disturbances. This condition predominantly manifests as right heart failure, severely impacting quality of life and life expectancy. Macrophages, as one of the most prevalent innate immune cells, have been increasingly recognized for their crucial role in the pathogenesis of HAPH. The low-pressure and hypoxic environment, along with other etiological factors, lead to metabolic abnormalities in tissue cells and the microenvironment. This results in increased secretion of chemokines, cytokines, and growth factors in the microenvironment, which promote the proliferation of tissue-resident macrophages and the differentiation of monocytes recruited from the blood into macrophages. This exacerbates the inflammatory cascade, further promoting cell proliferation, tissue repair, and inhibition of apoptosis. These processes contribute to the migration and proliferation of pulmonary arterial smooth muscle cells, endothelial cells, and fibroblasts, leading to vascular remodeling and ultimately the development of pulmonary arterial hypertension. This review examines the role of macrophage-mediated immune responses in high-altitude pulmonary arterial hypertension, with a focus on hypoxia as a key feature.
高原性肺动脉高压（HAPH）是一种以肺动脉压力升高超过正常生理值为特征的病症，其由高原低压、缺氧环境、遗传易感性、免疫功能障碍和神经源性紊乱共同作用所致。这种病症主要表现为右心衰竭，严重影响生活质量和预期寿命。巨噬细胞作为最普遍的固有免疫细胞之一，其在HAPH发病机制中的关键作用日益受到认可。低压和缺氧环境以及其他病因导致组织细胞和微环境出现代谢异常。这致使微环境中趋化因子、细胞因子和生长因子的分泌增加，进而促进组织驻留巨噬细胞的增殖以及从血液招募而来的单核细胞分化为巨噬细胞。这加剧了炎症级联反应，进一步促进细胞增殖、组织修复并抑制细胞凋亡。这些过程促使肺动脉平滑肌细胞、内皮细胞和成纤维细胞迁移和增殖，导致血管重塑并最终引发肺动脉高压。本综述探讨巨噬细胞介导的免疫反应在高原性肺动脉高压中的作用，重点关注缺氧这一关键特征。
