Open AccessKcnk3 dysfunction exaggerates the development of pulmonary hypertension induced by left ventricular pressure overload
Author(s) -
Mélanie Lambert,
Pedro MendesFerreira,
MariaRosa Ghigna,
Hélène Le Ribeuz,
Rui Adão,
Angèle Boët,
Véronique Capuano,
Catherine RückerMartin,
Carmen BrásSilva,
Rozenn Quarck,
Valérie Domergue,
JeanLuc Vachiéry,
Marc Humbert,
Frédéric Perros,
David Montani,
Fabrice Antigny
Publication year - 2021
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvab016
Subject(s) - medicine , ventricle , cardiology , pulmonary hypertension , pressure overload , lung , pulmonary artery , right ventricular hypertrophy , ventricular remodeling , muscle hypertrophy , heart failure , cardiac hypertrophy
Pulmonary hypertension (PH) is a common complication of left heart disease (LHD, Group 2 PH) leading to right ventricular (RV) failure and death. Several loss-of-function (LOF) mutations in KCNK3 were identified in pulmonary arterial hypertension (PAH, Group 1 PH). Additionally, we found that KCNK3 dysfunction is a hallmark of PAH at pulmonary vascular and RV levels. However, the role of KCNK3 in the pathobiology of PH due to LHD is unknown.
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