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Activin-A Regulates Bone Morphogenetic Protein Signaling in Pulmonary Endothelial Cells Without Affecting Bone
Benjamin J Dunmore1,2, Nobuhiro Kikuchi1,2,3, Wei Li1,2
1Victor Phillip Dahdaleh Heart and Lung Research Institute University of Cambridge Cambridge UK.
None:
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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