Nat Commun:肺动脉高压的内皮细胞中activin-A/BMPR2通路被异常激活

2021-03-26 xiaozeng MedSci原创

肺动脉高压(PAH)是一种罕见的进行性的致命疾病,全球每100万人中约有15至50例。

肺动脉高压(PAH)是一种罕见的进行性的致命疾病,全球每100万人中约有15至50例。持续性的肺动脉高压会导致右心室肥大,并最终导致右心衰竭。

由于目前该疾病的治疗选择仍有限,因此开发新的治疗策略显得迫在眉睫。PAH的病理特征在于病理性肺动脉的功能重塑。然而其详细的分子机制仍有待阐明。既往研究显示,内皮细胞(EC)功能障碍,如血管生成失调、细胞增殖和凋亡的非正常增加等,已被证实为该疾病的主要原因之一。

该研究描述了在血管性高血压中内皮血管分泌的作用。通过分析肺毛细血管内皮细胞中高表达的基因,研究人员发现,inhibin-β-A(抑制素-β-A)是由肺毛细血管产生的血管分泌因子。内皮细胞inhibin-β-A的过量产生能够以自分泌方式行使activin-A(激活素-A)的功能并损害了内皮功能。机制研究显示,activin-A能够诱导BMPR2(2型骨形态发生蛋白受体)的内化并靶向溶酶体途径的降解作用,并最终导致内皮细胞信号的缺乏。

抑制素-β-A为肺毛细血管的高表达基因

值得注意的是,相比于从正常对照的肺部分离内皮细胞,从特发性肺动脉高压患者的肺部分离出的内皮细胞显示出了更高的inhibin-β-A表达水平并产生更多的activin-A。当小鼠内皮细胞的activin-A/BMPR2通路被过度驱动时,会加剧缺氧诱导的肺动脉高压,而条件性敲除内皮细胞中的inhibin-β-A则能够阻止肺动脉高压的发展。


总而言之,该研究结果揭示,内皮细胞中activin-A/BMPR2通路的失调对于肺动脉高压的发展起着关键作用,因此inhibin-β-A/activin-A可能是该疾病的潜在药物治疗靶标。


原始出处:

Ryanto, G.R.T., Ikeda, K., Miyagawa, K. et al. An endothelial activin A-bone morphogenetic protein receptor type 2 link is overdriven in pulmonary hypertension. Nat Commun 12, 1720 (19 March 2021).

 

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    2021-10-15 liuli5079
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    2021-07-14 HNYYM
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    2021-07-16 liye789132251
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    2021-03-31 1436749007

    学到了很多东西谢谢老师

    0

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    2021-03-28 1436749007

    学到了很多东西谢谢老师

    0

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    2021-03-27 1436749007

    学到了很多谢谢老师

    0

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    2021-03-27 明天jing

    肺动脉高压表面是罕见病,事实上临床上并不少见,治疗药物虽然有一些,但是整体仍然不理解,可能未来需要采用综合治疗措施。

    0

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JAHA:肺动脉高压患者缺血性卒中预后的性别差异

PH与住院死亡率没有显著的相关性,但与住院时间延长和不良出院结局相关。男性PH患者比女性PH患者更有可能住院期间死亡。

JAHA:TNFRSF13B基因c.226G>A(p.Gly76Ser)是肺动脉高压患者新型致病突变

TNFRSF13B基因p.Gly76Ser变异体是PAH患者新型候选致病基因变异体。

Arthritis Rheumatol:DETECT算法可准确预测系统性硬化症患者的肺动脉高压风险

肺动脉高压(PAH)是导致系统性硬化症患者死亡的主要原因之一