ArticleHepatology (Baltimore, Md.)2021
High Mobility Group Box 1 Release by Cholangiocytes Governs Biliary Atresia Pathogenesis and Correlates With Increases in Afflicted Infants.
Article in Hepatology (Baltimore, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- IL‑17AInternational journal of molecular medicine · 2026Article
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- Biliary atresia: Rotavirus amplification of lipopolysaccharide/toll-like receptor 4 by mediating MMP7 upregulation through NF-κB.Pediatric research · 2025Article
- Investigating the potential role of miR-451a as a tumor suppressor in immunogenic cell death induction and dendritic cell maturation in colorectal cancer cell lines.Cancer cell international · 2025Article
- Immune and genetic landscapes of biliary atresia: a pathway to precision medicine.BMC pediatrics · 2025Article
- A nomogram model based on routine serum markers for predicting the occurrence of primary cholangitis after Kasai operation for biliary atresia.Translational pediatrics · 2025Article
- Protective effects of cilostazol via the HNF1α/FXR signalling pathway and anti-apoptotic mechanisms in a rat model of estrogen-induced intrahepatic cholestasis.Scientific reports · 2024Article
- Specific binding sites on Rhesus rotavirus capsid protein dictate the method of endocytosis inducing the murine model of biliary atresia.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Accurate prediction of biliary atresia with an integrated model using MMP-7 levels and bile acids.World journal of pediatrics : WJP · 2024Article
- Targeting ferroptosis and ferritinophagy: new targets for cardiovascular diseases.Journal of Zhejiang University. Science. B · 2024Review
- Association between serum HMGB1 elevation and early pediatric acute respiratory distress syndrome: a retrospective study of pediatric living donor liver transplant recipients with biliary atresia in China.BMC anesthesiology · 2023Article
- Necroptosis of macrophage is a key pathological feature in biliary atresia via GDCA/S1PR2/ZBP1/p-MLKL axis.Cell death & disease · 2023Article
- Sterile inflammation in liver transplantation.Frontiers in medicine · 2023Review
- Review
- 18β-Glycyrrhetinic Acid Protects against Cholestatic Liver Injury in Bile Duct-Ligated Rats.Antioxidants (Basel, Switzerland) · 2022Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- The versatility of macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2022Review
- Genetic Factors and Their Role in the Pathogenesis of Biliary Atresia.Frontiers in pediatrics · 2022Review
- Serum Relmβ combined with abdominal signs may predict surgical timing in neonates with NEC: A cohort study.Frontiers in pediatrics · 2022Article
- A joint transcriptional regulatory network and protein activity inference analysis identifies clinically associated master regulators for biliary atresia.Frontiers in pediatrics · 2022Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsBiliary atresia (BA) is a devastating cholangiopathy of infancy. Upon diagnosis, surgical reconstruction by Kasai hepatoportoenterostomy (HPE) restores biliary drainage in a subset of patients, but most patients develop fibrosis and progress to end-stage liver disease requiring liver transplantation for survival. In the murine model of BA, rhesus rotavirus (RRV) infection of newborn pups results in a cholangiopathy paralleling that of human BA. High-mobility group box 1 (HMGB1) is an important member of the danger-associated molecular patterns capable of mediating inflammation during infection-associated responses. In this study, we investigated the role of HMGB1 in BA pathogenesis. APPROACH AND
resultsIn cholangiocytes, RRV induced the expression and release of HMGB1 through the p38 mitogen-activated protein kinase signaling pathway, and inhibition of p38 blocked HMGB1 release. Treatment of cholangiocytes with ethyl pyruvate suppressed the release of HMGB1. Administration of glycyrrhizin in vivo decreased symptoms and increased survival in the murine model of BA. HMGB1 levels were measured in serum obtained from infants with BA enrolled in the PROBE and START studies conducted by the Childhood Liver Disease Research Network. High HMGB1 levels were found in a subset of patients at the time of HPE. These patients had higher bilirubin levels 3 months post-HPE and a lower survival of their native liver at 2 years.
conclusionsThese results suggest that HMGB1 plays a role in virus induced BA pathogenesis and could be a target for therapeutic interventions in a subset of patients with BA and high HMGB1.
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