Helen M. Arthur

This study develops bispecific antibodies that activate the ALK1-BMPRII pathway, reducing AVMs and improving symptoms in HHT mouse models.

This study identifies CDK6-driven cell cycle acceleration in endothelial cells as a driver of arteriovenous malformations in HHT, suggesting CDK4/6 inhibitors as potential therapeutic options.

This study shows that reduced endoglin in bone marrow endothelial cells causes vascular remodeling and hematopoietic changes, similar to those in hereditary hemorrhagic telangiectasia.

This study shows that inhibiting TOR and ERK pathways in endoglin mutant zebrafish reduces vascular abnormalities associated with HHT.

The paper shows that arterial endoglin (ENG) is not necessary to prevent arteriovenous malformations (AVMs), as specific loss of ENG in venous and capillary endothelium resulted in AVM frequency similar to pan-endothelial loss.