ALK1 Loss Results in Vascular Hyperplasia in Mice and Humans Through PI3K Activation

2018103 citationsJournal Articlebronze Open Access

Authors

Elisenda Alsina‐Sanchís · Institut Català d'Oncologia

Yaiza García-Ibáñez · Institut d'Investigació Biomédica de Bellvitge

Ana M. Figueiredo · Institut Català d'Oncologia

Carla Riera‐Domingo · Institut Català d'Oncologia

Albert Figueras · Institut d'Investigació Biomédica de Bellvitge

Xavier Matías‐Guiu · Bellvitge University Hospital

Oriol Casanovas

Abstract

Overall, our results indicate that the BMP9/ALK1 hub critically mediates vascular quiescence by limiting PI3K signaling and suggest that PI3K inhibitors could be used as novel therapeutic agents to treat hereditary hemorrhagic telangiectasia.

Topics & Keywords

Vascular Anomalies and Treatments Vascular Malformations and Hemangiomas Coagulation, Bradykinin, Polyphosphates, and Angioedema

UN Sustainable Development Goals

Good health and well-being

Publication Details

Published in: Arteriosclerosis Thrombosis and Vascular Biology

Volume 38, Issue 5, pp. 1216-1229

DOI: 10.1161/atvbaha.118.310760

Field-Weighted Citation Impact: 6.41