ArticlePediatric research2026
SULT2B1 promotes cholangiocyte epithelial-mesenchymal transition via Wnt/β-catenin/MMP7 pathway in biliary atresia.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Therapeutic equivalence of intermittent and continuous phototherapy for neonatal jaundice: a systematic review & meta-analysis with regression and trial sequential analysis.European journal of pediatrics · 2026Pooled it
- Elevated serum creatinine over the first week of life and mortality risk in extremely preterm neonates: a secondary analysis of the Preterm Erythropoietin Neuroprotection Trial (PENUT).Pediatric nephrology (Berlin, Germany) · 2026Trial
- SULT2B1 promotes cholangiocyte epithelial-mesenchymal transition in biliary atresia: one baby step or a giant leap in the pathogenesis of biliary atresia?Pediatric research · 2026Article
- Quantifying perioperative risk in congenital hypertrophic pyloric stenosis with pyloric index.Pediatric research · 2026Article
- Flat lines in survival from out-of-hospital pediatric cardiac arrest: making the case for bold reform in prehospital care and resuscitation.Pediatric research · 2026Article
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review.Frontiers in cell and developmental biology · 2026Review
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10 authors.
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Abstract
backgroundBiliary atresia (BA) is a severe neonatal disease characterized by obstruction of the biliary system and hepatic fibrosis. Epithelial-mesenchymal transition (EMT) occurs during the development of liver fibrosis in BA. However, the molecular mechanism that promotes elevated MMP7 expression and mediates the EMT process remains unknown. SULT2B1 has been shown to be involved in the intrahepatocellular EMT process, but its role in BA remains unknown.
methodsIn this study, we found that SULT2B1 was overexpressed in BA livers. The increased expression of SULT2B1 exhibited a high association with the severity of fibrosis and poor prognosis in BA, and it was significantly correlated with the MMP7-mediated EMT in cholangiocytes. Further study showed that the abnormal high expression of SULT2B1 was located in cholangiocytes in BA, which was consistent with the pattern of MMP7. In vitro, upon the treatment of TGF-β1, SULT2B1 was overexpressed and promoted the EMT process via the Wnt/β-catenin/MMP7 pathway in a human intrahepatic bile duct epithelial cell line. Silencing of SULT2B1 expression blocked Wnt/β-catenin/MMP7-mediated cholangiocyte EMT.
resultsSULT2B1 was overexpressed in BA livers and correlated with fibrosis severity and poor prognosis. Its expression was associated with MMP7-mediated EMT in cholangiocytes, with overexpression localized similarly to MMP7. TGF-β1 induced SULT2B1 overexpression, activating the Wnt/β-catenin/MMP7 pathway to promote EMT, while SULT2B1 silencing inhibited this process.
conclusionInhibition of the SULT2B1/Wnt/β-catenin/MMP7 axis may represent a potential therapeutic strategy for BA. IMPACT: EMT of cholangiocytes in BA is an important process in the development of biliary obstruction and liver fibrosis. SULT2B1 was a key molecule involved in regulating cholangiocyte EMT and liver fibrosis processes in BA. SULT2B1 induced by TGF-β1 up-regulated MMP7 and promoted EMT in Cholangiocytes. Blockage of the SULT2B1/Wnt/β-catenin/MMP7 axis may be a new therapeutic strategy to relieve BA liver fibrosis.
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