低氧性肺動脈高壓（HAPH）常發(fā)于高原地區(qū)人群，其發(fā)病機制復雜，主要特點是持續(xù)性血管收縮與不可逆血管重塑，隨著肺動脈狹窄引起肺血管阻力與肺動脈平均壓力的逐漸增加，部分壓力由右心室代償，進而導致右心室發(fā)生結構與功能的改變，最終發(fā)生心衰甚至死亡。目前，臨床上治療肺動脈高壓的藥物主要包括前列環(huán)素類似物和前列環(huán)素受體激動劑、內皮素受體拮抗劑、磷酸二酯酶-5抑制劑和可溶性鳥苷酸環(huán)化酶抑制劑，這些藥物僅能夠抑制血管收縮或促進血管擴張，對血管進行調控，無法根治肺動脈高壓疾??；而細胞死亡是指細胞在一系列有序的生物化學和形態(tài)學的變化下，最終失去其結構和功能，無法繼續(xù)正常運作的過程，包括細胞凋亡、鐵死亡、銅死亡、氧死亡、自噬等途徑。簡要介紹不同細胞死亡方式與HAPH發(fā)生發(fā)展的關系以及潛在的相關藥物，為其潛在的治療靶點提供思路。

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

國家自然科學基金資助項目（32060088，82060786，82360831）;國家自然科學基金面上項目（82374148）