Contribution of transient receptor potential canonical channels in human and experimental pulmonary arterial hypertension
Bastien Masson, Anaïs Saint‐Martin Willer, Mary Dutheil, Lucille Penalva, Hélène Le Ribeuz, Kristelle El Jekmek, Yann Ruchon, Sylvia Cohen‐Kaminsky, Jessica Sabourin, Marc Humbert, Olaf Mercier, David Montani, Véronique Capuano, Fabrice Antigny
Abstract
TRPC3 is increased in human and experimental pulmonary arterial hypertension (PAH). In PAH pulmonary arterial smooth muscle cells, TRPC3 participates in the aberrant store-operated Ca 2+ entry contributing to their pathological cell phenotypes (exacerbated proliferation, enhanced migration, apoptosis resistance, and vasoconstriction). Pharmacological in vivo inhibition of TRPC3 reduces the development of experimental PAH. Even if other TRPC acts on PAH development, our results prove that TRPC3 inhibition could be considered as an innovative treatment for PAH.