ArticleBMC gastroenterology2012
High mobility group B1 impairs hepatocyte regeneration in acetaminophen hepatotoxicity.
Article in BMC gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 63 citations in OpenAlex.
- Absence of IκBβ/NFκB signaling does not attenuate acetaminophen-induced hepatic injury.Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- Molecular pathogenesis of acetaminophen-induced liver injury and its treatment options.Journal of Zhejiang University. Science. B · 2022Review
- High Mobility Group Box 1: Biological Functions and Relevance in Oxidative Stress Related Chronic Diseases.Cells · 2022Review
- APAP-Induced IκBβ/NFκB Signaling Drives Hepatic Il6 Expression and Associated Sinusoidal Dilation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Enzyme-activated near-infrared fluorogenic probe with high-efficiency intrahepatic targeting ability for visualization of drug-induced liver injury.Chemical science · 2021Article
- Liver regeneration and inflammation: from fundamental science to clinical applications.Nature reviews. Molecular cell biology · 2021Review
- Mechanisms and pathophysiological significance of sterile inflammation during acetaminophen hepatotoxicity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Review
- Time to Develop Therapeutic Antibodies Against Harmless Proteins Colluding with Sepsis Mediators?ImmunoTargets and therapy · 2020Review
- Role of High-Mobility Group Box-1 in Liver Pathogenesis.International journal of molecular sciences · 2019Review
- Liver Regeneration after Acetaminophen Hepatotoxicity: Mechanisms and Therapeutic Opportunities.The American journal of pathology · 2019Review
- DAMPs and sterile inflammation in drug hepatotoxicity.Hepatology international · 2019Review
- Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.Journal of clinical and translational research · 2017Article
- Mechanistic Modelling of Drug-Induced Liver Injury: Investigating the Role of Innate Immune Responses.Gene regulation and systems biology · 2017Article
- HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis.International journal of inflammation · 2017Review
- HMGB1 and Extracellular Histones Significantly Contribute to Systemic Inflammation and Multiple Organ Failure in Acute Liver Failure.Mediators of inflammation · 2017Review
- Ionizing Radiation Induces HMGB1 Cytoplasmic Translocation and Extracellular Release.Guo ji fang she yi xue he yi xue za zhi = International journal of radiation medicine and nuclear medicine · 2016Article
- Improved prescription of taohechengqi-tang alleviates D-galactosamine acute liver failure in rats.World journal of gastroenterology · 2016Article
- Ethyl pyruvate is a novel anti-inflammatory agent to treat multiple inflammatory organ injuries.Journal of inflammation (London, England) · 2016Review
- Necrotic myocardial cells release damage-associated molecular patterns that provoke fibroblast activation in vitro and trigger myocardial inflammation and fibrosis in vivo.Journal of the American Heart Association · 2015Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcetaminophen (APAP) overdose induces massive hepatocyte necrosis. Necrotic tissue releases high mobility group B1 (HMGB1), and HMGB1 contributes to liver injury. Even though blockade of HMGB1 does not protect against APAP-induced acute liver injury (ALI) at 9 h time point, the later time points are not studied and the role of HMGB1 in APAP overdose is unknown, it is possible that neutralization of HMGB1 might improve hepatocyte regeneration. This study aims to test whether blockade of HMGB1 improves hepatocyte regeneration after APAP overdose.
methodsMale C57BL/6 mice were treated with a single dose of APAP (350 mg/kg). 2 hrs after APAP administration, the APAP challenged mice were randomized to receive treatment with either anti-HMGB1 antibody (400 μg per dose) or non-immune (sham) IgG every 24 hours for a total of 2 doses.
results24 hrs after APAP injection, anti-HMGB1 therapy instead of sham IgG therapy significantly improved hepatocyte regeneration microscopically; 48 hrs after APAP challenge, the sham IgG treated mice showed 14.6% hepatic necrosis; in contrast, blockade of HMGB1 significantly decreased serum transaminases (ALT and AST), markedly reduced the number of hepatic inflammatory cells infiltration and restored liver structure to nearly normal; this beneficial effect was associated with enhanced hepatic NF-κB DNA binding and increased the expression of cyclin D1, two important factors related to hepatocyte regeneration.
conclusionHMGB1 impairs hepatocyte regeneration after APAP overdose; Blockade of HMGB1 enhances liver recovery and may present a novel therapy to treat APAP overdose.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.