Activin-A Regulates Bone Morphogenetic Protein Signaling in Pulmonary Endothelial Cells Without Affecting Bone Morphogenetic Protein Type-II Receptor Expression.

IF 2.2 4区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

Pulmonary Circulation Pub Date : 2025-05-05 eCollection Date: 2025-04-01 DOI:10.1002/pul2.70095

Benjamin J Dunmore, Nobuhiro Kikuchi, Wei Li, Paul D Upton, Nicholas W Morrell

引用次数: 0

Abstract

Activin-A is elevated in pulmonary arterial hypertension (PAH) patients, and reportedly suppresses BMPR-II. This suggests one mechanism of action for PAH drug, sotatercept, an activin-ligand trap. However, we were unable to confirm that activin-A reduces BMPR-II in pulmonary endothelial cells. Thus, it seems unlikely that sotatercept influences BMPR-II or PAH via this mechanism.

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激活素a在不影响骨形态发生蛋白ii型受体表达的情况下调控肺内皮细胞骨形态发生蛋白信号转导

激活素a在肺动脉高压（PAH）患者中升高，据报道可抑制BMPR-II。这表明多环芳烃药物sotaterept的作用机制是激活素-配体陷阱。然而，我们无法证实激活素- a降低肺内皮细胞的BMPR-II。因此，sotaterept似乎不太可能通过这种机制影响BMPR-II或PAH。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Pulmonary Circulation Medicine-Pulmonary and Respiratory Medicine

CiteScore

4.20

自引率

11.50%

发文量

153

审稿时长

15 weeks

期刊介绍： Pulmonary Circulation''s main goal is to encourage basic, translational, and clinical research by investigators, physician-scientists, and clinicans, in the hope of increasing survival rates for pulmonary hypertension and other pulmonary vascular diseases worldwide, and developing new therapeutic approaches for the diseases. Freely available online, Pulmonary Circulation allows diverse knowledge of research, techniques, and case studies to reach a wide readership of specialists in order to improve patient care and treatment outcomes.