肺动脉高压（PAH）是一种临床罕见病，其发病机制尚未完全阐明。骨形成蛋白（BMP）信号通路是参与PAH发生发展的重要通路之一。我中心前期工作发现，PAH患者血浆BMP7水平较对照组显著升高，且在野百合碱诱导的PAH模型大鼠肺组织中BMP7表达水平也显著高于对照大鼠；异常升高的BMP7增强肺动脉平滑肌细胞的增殖和迁移能力，这表明BMP7可能参与肺血管重构和PAH的发生发展。我们前期研究还证实了BMP7的表达水平受DNA甲基化调控，但是PAH患者的调控机制是否存在异同仍未知。基于此，本研究从体内体外水平探究肺动脉高压致病因素作用下表观遗传学BMP7基因表达调控的影响及相应分子机制，以及高表达的BMP7对PAH肺血管重构的影响，进一步评估其与患者不良预后的相关性。BMP7有望成为PAH新靶点，为探究PAH的发生发展提供新思路，为药物干预提供潜在靶点。

Pulmonary arterial hypertension(PAH) is a rare clinical disease, the pathogenesis of which remains unclear. Bone morphogenetic protein (BMP) signal plays a significant role in the development of PAH. Our center has found that the plasma levels of BMP7 are dramatically higher compared to controls, which could also applied to the lung tissue of PAH model (MCT) rat. The abnormal elevated BMP7 increase the proliferation and migration of pulmonary artery smooth muscle cells.These results indicate that BMP7 may participate in the pulmonary vascular remodeling and the development of PAH. We also detect that BMP7 expression levels may regulated by methylation of DNA, though little is known about the similarities and difference in regulatory mechanism that control BMP7 expression. Based on above data, we explore the regulation of DNA methylation effect and the underlying molecular mechanisms of BMP7 in vivo and in vitro, as well as the effect of BMP7 on pulmonary vascular remodeling and prognosis significance in pulmonary arterial hypertension. BMP7 may become a promising target of PAH, which may help illustrate the development of PAH and provide potential targets for drug intervention.