缺氧诱导丝裂原因子与肺动脉高压

缺氧诱导丝裂原因子（hypoxia—induced mitogenic factor，HIMF）是近年来从慢性缺氧致肺动脉高压小鼠模型的肺组织中发现的一种分泌型蛋白，于肺组织中被缺氧诱导表达，因其能促进小鼠肺微血管平滑肌细胞的增殖而得名，是肺组织特异性生长因子，又名发现于炎症区域1（found in inflammatory zone1，FIZZ1）或抵抗素样分子α（resistin-like molecule—α，RELM—α）。HIMF／FIZZ1／RELM—α具有促有丝分裂、血管收缩、血管再生和诱导细胞迁移、趋化性、抗细胞凋亡、炎症因子样作用等多种生物学功能。研究发现HIMF通过引起肺血流动力学改变，血流阻力增加，肺动脉压增高等不同的方式参与肺血管收缩及重塑。HIMF的各种生物学特性证明其和肺动脉高压，尤其是慢性缺氧性肺动脉高压的发病机制有密切的联系，而这对肺动脉高压的治疗是非常重要的。下面就HIMF与肺动脉高压的相互联系作一归纳、总结。

Hypoxia-induced mitogenic factor and pulmonary hypertension

Hypoxia-induced mitogenic factor （HIMF）,a secreted protein,is discovered in a mouse model of hypoxia-induced pulmonary hypertension and is inducibled by hypoxia in lung. As a lung-specific growth factor, HIMF can stimulates rat pulmonary microvascular smooth muscle cell （RPSM） proliferation. HIMF also known as FIZZ1/RELM-α. Researches suggested that HIMF possesses mitogenic, vasoconstrictive, angiogenic, and migration, antiapoptotic, chemokine-like, inflammatory properties. HIMF can induce the vascular and hemodynamic changes of PAH, increase blood flow resistance,and at last, increase the pulmonary artery pressure. Through these different ways, HIMF participate in pulmonary vasoconstriction and pulmonary vascular remodeling. These biological functions HIMF has shows that it is very close contact with the pathogenesis of pulmonary hypertension （PH）, especially the hypoxia-induced pulmonary hypertension （HPH）, which is very important to the therapeutic strategy for the diseases. Here is a induction of the relationship between HIMF and PH.