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The epithelial cell that lines the bile ducts.
References in periodicals archive ?
Cyclooxygenase-2 (COX-2) plays a role in the pathogenesis of CCA, activating growth factors that promotes cholangiocyte growth, such as MAPK, epidermal growth factor receptor (EGFR) and interleukin 6 (IL-6), concluded the company.
In the latter, the upregulation of VEGFR-3 and secretion of VEGF-C ligand have appeared to mediate the adaptive proliferative response of cholangiocyte to BDL-induced early cholestatic liver injury via an autocrine mechanism that involves activation of inositol 1,4,5-triphosphate/[Ca2+]i/protein kinase C alpha and phosphorylation of Src/extracellular signal-regulated kinases 1/2 [18].
sup][17] We have learned that estrogens and their receptors influence the pathophysiology of cholangiocytes and that this mainly occurs during experimental and human conditions characterized by cholangiocyte injury and proliferation.
Polycystic liver diseases: Congenital disorders of cholangiocyte signaling.
MAPK signaling contributes to rotaviral-induced cholangiocyte injury and viral replication.
Vascular endothelial growht factor stimulates rat cholangiocyte proliferation via an autocrine mechanism.
Addressing the hypothesis that XBP1 and ER stress may contribute to the molecular pathology of primary sclerosing cholangitis (PSC) via affecting cholangiocyte biology.
Objective: Cholangiopathies represent a diverse group of diseases affecting cholangiocytes which are the main cell type of the biliary tract.
Molecular hydrogen attenuates hypoxia/reoxygenation injury of intrahepatic cholangiocytes by activating Nrf2 expression.
Hepatoblasts are bipotential liver progenitor cells that can differentiate into either hepatocytes, cells that comprises the majority of liver tissue, or cholangiocytes, epithelial cells of the bile duct.
The late changes include periportal fibrosis with irregularity of lining cholangiocytes of the intrahepatic ducts represented by vacuolization, nuclear pyknosis, infiltration by inflammatory cells, thickening, progressive atrophy and disappearance of ducts.