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Pancreatitis: correcting CFTR expression and function as a promising effective treatment.
Paramita Sarkar1, Wei-Yin Lin1, Ava Movahed Abtahi1
1The Epithelial Signaling and Transport Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MA, United States.
Frontiers in Physiology
|May 18, 2026
Summary
Impaired function of the cystic fibrosis transmembrane conductance regulator (CFTR) channel is central to pancreatitis. CFTR modulators, used for cystic fibrosis, may offer new pancreatitis treatments.
Area of Science:
- Gastroenterology and Hepatology
- Cell Biology
- Medical Research
Background:
- The exocrine pancreas relies on acinar cells for enzyme secretion and ductal cells for alkaline fluid and bicarbonate secretion.
- Ductal secretion, regulated by the cystic fibrosis transmembrane conductance regulator (CFTR) channel, is crucial for pancreatic protection and digestive enzyme transport.
- Pancreatitis, a prevalent pancreatic disease, is characterized by ductal injury and inflammation, with impaired CFTR function implicated across all forms.
Purpose of the Study:
- To review evidence linking alterations in CFTR expression and activity to pancreatitis pathogenesis.
- To explore the potential of CFTR modulators as therapeutic strategies for pancreatitis.
Main Methods:
- Literature review of studies on CFTR function in pancreatic physiology and pathophysiology.
- Analysis of existing data on CFTR modulators in cystic fibrosis treatment.
Main Results:
- Growing evidence implicates dysfunctional CFTR as a common factor in pancreatitis development.
- CFTR correctors and potentiators are approved and effective for cystic fibrosis treatment.
Conclusions:
- Altered CFTR expression and activity are key events in the pathogenesis of pancreatitis.
- CFTR modulators represent a promising therapeutic avenue for pancreatitis, warranting further investigation.
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