Role of KCNK3 Dysfunction in Dasatinib-associated PAH and Endothelial Cell Dysfunction

Hélène Le Ribeuz; Anaïs Saint‐Martin Willer; B. Chevalier; María Sancho; Bastien Masson; Mélanie Eyries; Vincent Jung; Ida Chiara Guerrera; Mary Dutheil; Kristelle El Jekmek; Loann Laubry; Gilles Carpentier; Francisco Pérez‐Vizcaíno; Ly Tu; Christophe Guignabert; Marie‐Camille Chaumais; Christine Péchoux; Marc Humbert; Alexandre Hinzpeter; Olaf Mercier; Véronique Capuano; David Montani; Fabrice Antigny

doi:10.1165/rcmb.2023-0185oc

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Abstract

Pulmonary arterial (PA) hypertension (PAH) is a severe cardiopulmonary disease that may be triggered by exposure to drugs such as dasatinib or facilitated by genetic predispositions. The incidence of dasatinib-associated PAH is estimated at 0.45%, suggesting individual predispositions. The mechanisms of dasatinib-associated PAH are still incomplete. We discovered a

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Ribeuz et al. (2024) studied this question.

synapsesocial.com/papers/68e71ed9b6db64358769882b https://doi.org/10.1165/rcmb.2023-0185oc

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Role of KCNK3 Dysfunction in Dasatinib-associated PAH and Endothelial Cell Dysfunction

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Role of KCNK3 Dysfunction in Dasatinib-associated PAH and Endothelial Cell Dysfunction

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