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Camostat mesylate restores intestinal barrier integrity and attenuated protein loss in experimental protein-losing

Joowon Lee1, Chang Sik Cho2, Hyun Chul Jeong3

  • 1Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam, South Korea.

Biochemical Pharmacology
|November 21, 2025
PubMed

Insights

Camostat mesylate (CM) shows promise in treating protein-losing enteropathy (PLE) after the Fontan operation. This study found CM improved intestinal barrier function and clinical outcomes in both mouse models and human patients with Fontan-associated PLE.

Area of Science:

  • Gastroenterology
  • Cardiology
  • Pharmacology

Background:

  • Protein-losing enteropathy (PLE) is a severe complication of the Fontan operation for single-ventricle congenital heart disease.
  • Intestinal barrier dysfunction and lymphangiectasia are key features of PLE, with dysregulated protease activity implicated in its pathogenesis.

Purpose of the Study:

  • To investigate the therapeutic potential of camostat mesylate (CM), a protease inhibitor, for managing intestinal barrier dysfunction in protein-losing enteropathy (PLE).
  • To evaluate CM's efficacy in a dextran sulfate sodium (DSS)-induced colitis mouse model mimicking Fontan-associated PLE and in human patients.

Main Methods:

  • Established a DSS-induced colitis mouse model exhibiting PLE characteristics.
  • Administered oral camostat mesylate (CM) to mice and assessed intestinal damage and lymphangiectasia.
  • Utilized Caco-2 cell monolayers to evaluate CM's effect on barrier integrity markers (ZO-1, transepithelial electrical resistance).
  • Monitored fecal alpha-1 antitrypsin (A1AT) and serum albumin levels in a patient with Fontan-associated PLE treated with CM.

Main Results:

  • The DSS model showed hypoalbuminemia, elevated fecal A1AT, lymphangiectasia, and reduced EpCAM/claudin-7, mimicking PLE.
  • CM treatment significantly reduced weight loss, colon damage, and lymphangiectasia in the mouse model.
  • CM restored ZO-1 expression and transepithelial electrical resistance in DSS-challenged Caco-2 cells.
  • In a patient, CM treatment led to decreased fecal A1AT and increased serum albumin levels.

Conclusions:

  • Camostat mesylate effectively ameliorated intestinal barrier dysfunction and lymphangiectasia in a preclinical model of PLE.
  • Clinical data suggests CM improves key biomarkers and clinical outcomes in patients with Fontan-associated PLE.
  • Protease inhibition with camostat mesylate represents a promising therapeutic strategy for managing protein-losing enteropathy post-Fontan operation.

Keywords:
Animal modelCamostat mesylateFontan operationProtease inhibitorProtein-losing enteropathy

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