2025/06/02 by John M. Moran, John Moran, Courtney Pugh +12
Medicine · #Cystic Fibrosis Research Advances
paper · doi:10.1152/ajplung.00009.2025
openalex publication_date 2025/06/02 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/22
New research reveals that epithelial sodium channel (ENaC) overexpression in cystic fibrosis (CF) immune cells impairs macrophage function. Inhibiting ENaC increases cystic fibrosis transmembrane conductance regulator (CFTR) expression, normalizes reactive oxygen species production, improves autophagy, and reduces proinflammatory cytokine production. This suggests that ENaC modulation could be a novel therapeutic target for CF infection control, either alone or with CFTR modulators, offering new hope for patients not eligible for current treatments.