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抑制BMPER通过调节平滑肌肉细胞中的LRP1-YAP相互作用来缓解肺高血压

Hua Mao^1,2, Claire M Li^1,2, Bing Sun^1,2

¹Department of Medicine, Cardiovascular Research (H.M., C.M.L., B.S., L.X., X.P.), Baylor College of Medicine, Houston, TX.

Arteriosclerosis, thrombosis, and vascular biology

|September 18, 2025

概括

骨形态遗传蛋白结合性内皮调节器 (BMPER) 在肺动脉高血压 (PAH) 中升高,并驱动血管重塑. 抑制BMPER可能为PAH提供一种新的治疗策略.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
肺高血压研究肺高血压研究

背景情况:

骨形态遗传蛋白结合内皮调节器 (BMPER) 是一种分泌的蛋白质,对血管发育至关重要.
骨形态遗传蛋白 (BMP) 途径的突变与肺动脉高血压 (PAH) 有关.
在此之前,BMPER在PAH病原发生中的特定作用是未知的.

研究的目的:

研究1组肺动脉高血压中BMPER的表达和功能.
阐明BMPER影响肺血管重塑的机制.
评估针对PAH中BMPER的治疗潜力.

主要方法:

在人类PAH患者样本中评估了BMPER表达.
利用体内 (小鼠模型) 和体内方法来研究BMPER在血管重塑中的作用.
研究了BMPER对肺动脉平滑肌肉细胞增殖和右心室压力的影响.
研究了BMPER,YAP和LRP1.1之间的机械联系.

主要成果:

在PAH肺部,BMPER水平升高,与肺血管抵抗相关.
在小鼠中的BMPER枯竭减弱了肺血管重塑和降低了右心室压力.
在小鼠中,BMPER过度表达诱导了自发的PAH发展.
BMPER通过LRP1促进YAP激活,有助于肺动脉光滑肌肉细胞的增殖.

结论:

分泌的BMPER是PAH中肺血管重塑的关键调节剂.
BMPER的机制涉及通过LRP1.1调解的YAP激活.
抑制BMPER是肺动脉高血压的潜在新疗法策略.

关键词:

细胞的增殖细胞的增殖.内皮细胞是内皮细胞.高血压,肺部高血压,肺部高血压.缺氧缺氧是指缺氧的情况.血管改造血管改造血管改造

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