ArticlePediatric research2023
Potential therapeutic target of EGF on bile duct ligation model and biliary atresia children.
Article in Pediatric research, 2023. 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, 10 citations in OpenAlex.
- Systematic review of the mechanism and assessment of liver fibrosis in biliary atresia.Pediatric surgery international · 2024Pooled it
- Matrix Metalloproteinase 7 Mediates Epithelial-Mesenchymal Transition to Promote Liver Fibrosis Through E-cadherin/β-catenin Pathway in Biliary Atresia.International journal of molecular sciences · 2026Article
- Scar-associated macrophages and biliary epithelial cells interaction exacerbates hepatic fibrosis in biliary atresia.Pediatric research · 2026Article
- Global research trends in biliary atresia-related liver fibrosis: a bibliometric analysis (2000-2024).Frontiers in pediatrics · 2026Article
- EGFR activation in cholangiocytes promotes extrahepatic bile duct regeneration after injury.Hepatology communications · 2025Article
- Inflammatory factor CCL2 enhances the interaction between monocyte-macrophage cells and liver parenchymal cells to promote liver inflammation and fibrosis in biliary atresia.BMC pediatrics · 2025Article
- Suprabasin promotes gastric cancer liver metastasis via hepatic stellate cells-mediated EGF/CCL2/JAK2 intercellular signaling pathways.Oncogene · 2025Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe pathogenesis of liver fibrosis in biliary atresia (BA) is unclear. Epidermal growth factor (EGF) plays a vital role in liver fibrosis. This study aims to investigate the expression of EGF and the mechanisms of its pro-fibrotic effects in BA.
methodsEGF levels in serum and liver samples of BA and non-BA children were detected. Marker proteins of EGF signaling and epithelial-mesenchymal transition (EMT) in liver sections were evaluated. Effects of EGF on intrahepatic cells and the underlying mechanisms were explored in vitro. Bile duct ligation (BDL) mice with/without EGF antibody injection were used to verify the effects of EGF on liver fibrosis.
resultsSerum levels and liver expression of EGF elevated in BA. Phosphorylated EGF receptor (p-EGFR) and extracellular regulated kinase 1/2 (p-ERK1/2) increased. In addition, EMT and proliferation of biliary epithelial cells were present in BA liver. In vitro, EGF induced EMT and proliferation of HIBEpic cells and promoted IL-8 expression in L-02 cells by phosphorylating ERK1/2. And EGF activated LX-2 cells. Furthermore, EGF antibody injection reduced p-ERK1/2 levels and alleviated liver fibrosis in BDL mice.
conclusionEGF is overexpressed in BA. It aggravates liver fibrosis through EGF/EGFR-ERK1/2 pathway, which may be a therapeutic target for BA. IMPACT: The exact pathogenesis of liver fibrosis in BA is unknown, severely limiting the advancement of BA treatment strategies. This study revealed that serum and liver tissue levels of EGF were increased in BA, and its expression in liver tissues was correlated with the degree of liver fibrosis. EGF may promote EMT and proliferation of biliary epithelial cells and induce IL-8 overexpression in hepatocytes through EGF/EGFR-ERK1/2 signaling pathway. EGF can also activate HSCs in vitro. The EGF/EGFR-ERK1/2 pathway may be a potential therapeutic target for BA.
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