TABLE 2.

Signal pathways involved in the pathological process of biliary stenosis and their functions.

Pathological process	Signal pathways	Functions
Epithelial regeneration	Notch	Hepatocyte transdifferentiation; HPC proliferation and differentiation
	TGF-β	Hepatocyte transdifferentiation
	Wnt	Hepatic progenitor cell proliferation and differentiation
Inflammatory response	FXR	Immune cell activation, differentiation, and cytokine secretion; regulation of fibrosis progression
	VDR	Immune cell activation, differentiation, and cytokine secretion
	TGR5	Regulation of local inflammatory responses, epithelial apoptosis, and fibrosis progression
	TLR	Activation of downstream inflammatory pathways such as NF-κB to enhance inflammatory cytokine release
	PPAR	Negative regulatory role in maintaining biliary metabolic homeostasis and inhibiting inflammatory responses, mitigating excessive inflammation through transcriptional repression
	Hippo	Regulation of biliary epithelial cell proliferation and repair via modulation of YAP/TAZ activity; dysregulation closely associated with abnormal cholangiocyte proliferation and fibrosis
	Hedgehog	Participation in epithelial-mesenchymal crosstalk, regulation of ductular reaction and fibroblast activation, playing a dual role in balancing inflammation and repair after biliary injury
Fibrotic deposition	TGF-β	Promotion of hepatic stellate cell (HSC) activation via Smad-dependent signaling pathway, acting as a core driver of fibrosis formation
	Wnt	Regulation of biliary epithelial cell proliferation and epithelial-mesenchymal transition (EMT), synergizing with TGF-β signaling
	Notch	Modulation of differentiation status of HPCs and biliary tree stem/progenitor cells (BTSCs), critically regulating the balance between biliary regeneration and fibrosis
	PI3K/AKT	Involvement in cell survival and extracellular matrix (ECM) regulation
	TLR	Mediation of the interaction between immune-inflammatory responses and fibrosis