A pathological intestinal fibrosis model characterized by fibroblast activation and excessive extracellular matrix accumulation, resulting in tissue stiffening and structural deformation with activation of fibrosis-related signaling pathways.
This platform enables human-based in vitro evaluation of antifibrotic candidate compounds.
Intestinal fibrosis is a major complication of chronic inflammatory bowel diseases, particularly Crohn’s disease. Progressive fibroblast activation and excessive extracellular matrix (ECM) deposition lead to tissue stiffening, luminal narrowing, and ultimately stricture formation.
Despite advances in anti-inflammatory biologics, effective antifibrotic therapies remain an unmet clinical need, partly due to the lack of predictive human-relevant preclinical models.
Our human intestinal organoid–based fibrosis model recapitulates key pathological hallmarks of intestinal fibrogenesis in vitro:
By integrating epithelial organoids with stromal components, this platform reconstructs multicellular interactions that drive fibrotic remodeling in human intestine.
The model supports multi-layered characterization:
