Deficiency of Axl aggravates pulmonary arterial hypertension via BMPR2

Deficiency of Axl aggravates pulmonary arterial hypertension via BMPR2

Novoyatleva et al investigate the role of receptor tyrosine kinase Axl in Pulmonary arterial hypertension (PAH), finding that the small molecule inhibitor R428 reduces human pulmonary arterial smooth muscle cells proliferation and migration, but causes toxicity in human pulmonary arterial endothelia...

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Detalles Bibliográficos
Autores principales: Tatyana Novoyatleva, Nabham Rai, Baktybek Kojonazarov, Swathi Veeroju, Isabel Ben-Batalla, Paola Caruso, Mazen Shihan, Nadine Presser, Elsa Götz, Carina Lepper, Sebastian Herpel, Grégoire Manaud, Frédéric Perros, Henning Gall, Hossein Ardeschir Ghofrani, Norbert Weissmann, Friedrich Grimminger, John Wharton, Martin Wilkins, Paul D. Upton, Sonja Loges, Nicholas W. Morrell, Werner Seeger, Ralph T. Schermuly
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
Materias:
Biology (General)
QH301-705.5
Acceso en línea:https://doaj.org/article/9cdae1283c834b96804aa01aec8d92af
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Sumario:Novoyatleva et al investigate the role of receptor tyrosine kinase Axl in Pulmonary arterial hypertension (PAH), finding that the small molecule inhibitor R428 reduces human pulmonary arterial smooth muscle cells proliferation and migration, but causes toxicity in human pulmonary arterial endothelial cells. They further show that Axl enhances endothelial BMPR2 signaling, altogether providing insights into mechanisms of PAH.

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