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

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

doi:10.1002/pul2.70095

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

Pulm Circ. 2025 May 5;15(2):e70095. doi: 10.1002/pul2.70095. eCollection 2025 Apr.

Authors

Benjamin J Dunmore^{1

2}, Nobuhiro Kikuchi^{1

2

3}, Wei Li^{1

2}, Paul D Upton^{1

2}, Nicholas W Morrell^{1

2}

Affiliations

¹ Victor Phillip Dahdaleh Heart and Lung Research Institute University of Cambridge Cambridge UK.
² Department of Medicine, School of Clinical Medicine University of Cambridge Cambridge UK.
³ Department of Cardiovascular Medicine Tohoku University Graduate School of Medicine Sendai Japan.

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.

Publication types

Letter