General Capillary to Arterial Endothelial Cell Transition in Pulmonary Arterial Hypertension

标题：肺动脉中总毛细血管向动脉内皮细胞的转变 高血压 项目摘要 肺动脉高压(PAH)的特征是肺组织进行性增加。 血管阻力和闭塞性肺血管重塑导致右心肥厚， 失败和过早死亡。毛细血管内皮细胞(ECs)和血管内皮细胞丢失的机制 闭塞性血管病变的形成仍不清楚。我们的初步数据显示动脉 程序化在人类PAH患者和啮齿动物中很明显。我们假设一般的毛细血管内皮细胞 通过HIF-2、-CDK19/Sox17/Notch4信号通路调节动脉内皮细胞 PAH的发病机制。完成我们建议的研究将提供一种新的治疗策略 对PAH患者的有效治疗。

Title: General Capillary to Arterial Endothelial Cell Transition in Pulmonary Arterial Hypertension Project Summary Pulmonary arterial hypertension (PAH) is characterized by a progressive increase of pulmonary vascular resistance and obliterative pulmonary vascular remodeling that result in right heart hypertrophy, failure, and premature death. The underlying mechanisms of loss of capillary endothelial cells (ECs) and obliterative vascular lesion formation remain unclear. Our preliminary data showed that arterial programing was evident in human PAH patients and rodents. We hypothesize that general capillary ECs program to arterial ECs through HIF-2-Cdk19/Sox17/Notch4 signaling which contributes to the pathogenesis of PAH. Completing our proposed study will provide a novel therapeutic strategy for the effective treatment of PAH in patients.