Contribution of transient receptor potential canonical channels in human and experimental pulmonary arterial hypertension-Reference-Cited by-同舟云学术

Contribution of transient receptor potential canonical channels in human and experimental pulmonary arterial hypertension

Published:2023-08-01 Issue:2 Volume:325 Page:L246-L261
ISSN:1040-0605
Container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology
language:en
Short-container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology

Author:

Masson Bastien¹²^ORCID,Saint-Martin Willer Anais¹²,Dutheil Mary¹²³,Penalva Lucille¹²,Le Ribeuz Hélène¹²,El Jekmek Kristelle¹²,Ruchon Yann¹²³,Cohen-Kaminsky Sylvia¹²^ORCID,Sabourin Jessica⁴,Humbert Marc¹²⁵,Mercier Olaf¹²⁶,Montani David¹²⁵^ORCID,Capuano Véronique¹²³,Antigny Fabrice¹²^ORCID

Affiliation:

1. Faculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France

2. INSERM UMR_S 999, Hypertension pulmonaire: Physiopathologie et Innovation Thérapeutique, Hôpital Marie Lannelongue, Le Plessis-Robinson, France

3. Hôpital Marie Lannelongue, Groupe Hospitalier Paris Saint-Joseph, Le Plessis Robinson, France

4. INSERM UMR-S 1180, Signalisation et Physiopathologie Cardiovasculaire, Université Paris-Saclay, Châtenay-Malabry, France

5. Assistance Publique - Hôpitaux de Paris (AP-HP), Service de Pneumologie et Soins Intensifs Respiratoires, Centre de Référence de l’Hypertension Pulmonaire, Hôpital Bicêtre, Le Kremlin-Bicêtre, France

6. Service de Chirurgie Thoracique, Vasculaire et Transplantation Cardio-Pulmonaire, Hôpital Marie Lannelongue, Groupe Hospitalier Paris Saint Joseph, Le Plessis Robinson, France

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 Ca2+ 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.

Funder

Marie Lannelongue Hospital

Therapeutic Innovation Doctoral School

Agence Nationale de la Recherche

Institut National de la Santé et de la Recherche Médicale

University of Paris-Saclay | Ecoles doctorales, Université Paris-Saclay

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajplung.00011.2023