低氧性肺动脉高压(HPH)是以低氧性肺动脉收缩和低氧性肺血管重构引起的肺动脉压持续升高为特征的临床常见病症。细胞增殖与凋亡是肺血管重构中极其重要的一个环节,低氧诱导分子-Ⅰ、一氧化氮、一氧化碳、K+通道及5-羟色胺均参与并影响肺动脉平滑肌细胞的增殖及凋亡。本文就上述致低氧性肺动脉高压因素在肺血管重构中的机制及作用作一综述,为低氧性肺动脉高压的分子水平干预和早期康复措施介入提供新的靶点。 Hypoxic pulmonary hypertension (HPH) is a clinically common condition characterized by persistent hypoxia-induced pulmonary hypertension and hypoxic pulmonary vascular remodeling. Cell proliferation and apoptosis are extremely important in pulmonary vascular remodeling. Hypoxia-inducible molecule-Ⅰ, nitric oxide, carbon monoxide, K + channel and 5-HT all participate in and affect the proliferation and apoptosis of pulmonary artery smooth muscle cells. This review summarizes the mechanisms and effects of hypoxic pulmonary hypertension in pulmonary vascular remodeling and provides a new target for the intervention of molecular level and early rehabilitation measures for hypoxic pulmonary hypertension.