Inhibition of the sodium-dependent HCO₃^- transporter SLC4A4, produces a cystic fibrosis-like airway disease phenotype.

ABSTRACT: Bicarbonate secretion is a fundamental process involved in maintaining acid-base homeostasis. Disruption of bicarbonate entry into airway lumen, as has been observed in cystic fibrosis, produces several defects in lung function due to thick mucus accumulation. Bicarbonate is critical for correct mucin deployment and there is increasing interest in understanding its role in airway physiology, particularly in the initiation of lung disease in children affected by cystic fibrosis, in the absence of detectable bacterial infection. The current model of anion secretion in mammalian airways consists of CFTR and TMEM16A as apical anion exit channels, with limited capacity for bicarbonate transport compared to chloride. However, both channels can couple to SLC26A4 anion exchanger to maximise bicarb

SUBMITTER: Saint-Criq V 

PROVIDER: S-EPMC9173743 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature