Importance of ENaC-mediated sodium transport in alveolar fluid clearance using genetically-engineered mice.

Détails

Ressource 1Télécharger: Hummler_Planès09 - copie.pdf (190.76 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_A4A68D25B06B
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Importance of ENaC-mediated sodium transport in alveolar fluid clearance using genetically-engineered mice.
Périodique
Cellular physiology and biochemistry
Auteur(s)
Hummler E., Planès C.
ISSN
1421-9778
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
25
Numéro
1
Pages
63-70
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
The lung possesses specific transport systems that intra- and extracellularly maintain salt and fluid balance necessary for its function. At birth, the lungs rapidly transform into a fluid (Na(+))-absorbing organ to enable efficient gas exchange. Alveolar fluid clearance, which mainly depends on sodium transport in alveolar epithelial cells, is an important mechanism by which excess water in the alveoli is reabsorbed during the resolution of pulmonary edema. In this review, we will focus and summarize on the role of ENaC in alveolar lung liquid clearance and discuss recent data from mouse models with altered activity of epithelial sodium channel function in the lung, and more specifically in alveolar fluid clearance. Recent data studying mice with hyperactivity of ENaC or mice with reduced ENaC activity clearly illustrate the impaired lung fluid clearance in these adult mice. Further understanding of the physiological role of ENaC and its regulatory proteins implicated in salt and water balance in the alveolar cells may therefore help to develop new therapeutic strategies to improve gas exchange in pulmonary edema.
Mots-clé
Epithelial sodium channel, ENaC, CAP1, Channel-activating protease, Edema, Transgenic mice
Pubmed
Web of science
Open Access
Oui
Création de la notice
08/01/2010 18:28
Dernière modification de la notice
20/08/2019 16:10
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