低氧性肺动脉高压（HAPH）常发于高原地区人群，其发病机制复杂，主要特点是持续性血管收缩与不可逆血管重塑，随着肺动脉狭窄引起肺血管阻力与肺动脉平均压力的逐渐增加，部分压力由右心室代偿，进而导致右心室发生结构与功能的改变，最终发生心衰甚至死亡。目前，临床上治疗肺动脉高压的药物主要包括前列环素类似物和前列环素受体激动剂、内皮素受体拮抗剂、磷酸二酯酶-5抑制剂和可溶性鸟苷酸环化酶抑制剂，这些药物仅能够抑制血管收缩或促进血管扩张，对血管进行调控，无法根治肺动脉高压疾病；而细胞死亡是指细胞在一系列有序的生物化学和形态学的变化下，最终失去其结构和功能，无法继续正常运作的过程，包括细胞凋亡、铁死亡、铜死亡、氧死亡、自噬等途径。简要介绍不同细胞死亡方式与HAPH发生发展的关系以及潜在的相关药物，为其潜在的治疗靶点提供思路。

Hypoxic pulmonary hypertension often occurs in people in plateau areas, and its pathogenesis is complex, mainly characterized by continuous vascular constriction and irreversible vascular remodeling. As pulmonary artery stenosis causes the gradual increase of pulmonary vascular resistance and mean pulmonary artery pressure, part of the pressure is compensated by the right ventricle, which leads to structural and functional changes in the right ventricle, and eventually heart failure or even death. Clinically, the drugs used to treat pulmonary hypertension mainly include prostacyclin analogues, prostacyclin receptor agonists, endothelin receptor antagonists, phosphodiesterase-5 inhibitors and soluble guanylate cyclase inhibitors. These drugs can only inhibit vasoconstriction or promote vasodilation, regulate blood vessels, and cannot cure pulmonary hypertension. Cell death refers to the process in which cells eventually lose their structure and function and cannot continue to operate normally under a series of orderly biochemical and morphological changes, including apoptosis, iron death and other pathways. This article briefly reviewed the occurrence and development of cell death in hypoxic pulmonary hypertension, and provided ideas for potential therapeutic targets.

R972

国家自然科学基金资助项目（32060088，82060786，82360831）;国家自然科学基金面上项目（82374148）