ArticleGut2017
Signalling via the osteopontin and high mobility group box-1 axis drives the fibrogenic response to liver injury.
Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 83 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed, 138 citations in OpenAlex.
- HMGB1 links chronic liver injury to progenitor responses and hepatocarcinogenesis.The Journal of clinical investigation · 2018Trial
- Exosome-Associated Gene Network and the Role of SPP1 in Herpes Stromal Keratitis and the Therapeutic Modulation by Ursolic Acid.Investigative ophthalmology & visual science · 2026Article
- Integrative Multi-Omics Analysis Elucidates the Progressive Disease Landscape and Reveals Dynamic Protein Biomarkers for MASLD Surveillance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Extracellular Vesicles in Liver Disease: Redefining Diagnostic and Therapeutic Strategies.International journal of stem cells · 2026Review
- Serum osteopontin levels predict short-term outcomes in patients with hepatitis B-related acute-on-chronic liver failure.Journal of virus eradication · 2025Article
- Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.Annals of medicine · 2025Review
- Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Immune Dysfunction and Infection Risk in Advanced Liver Disease.Gastroenterology · 2025Review
- New insights into biomarkers and risk stratification to predict hepatocellular cancer.Molecular medicine (Cambridge, Mass.) · 2025Review
- Intra and inter-organ communication through extracellular vesicles in obesity: functional role of obesesomes and steatosomes.Journal of translational medicine · 2025Article
- HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- TREM2 in MASH: integrating lipid metabolism and immune response.Frontiers in immunology · 2025Review
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- Inflammatory biomarkers as cost-effective predictive tools in metabolic dysfunction-associated fatty liver disease.World journal of gastroenterology · 2024Review
- Osteokines in Nonalcoholic Fatty Liver Disease.Current obesity reports · 2024Review
- OPN-Mediated Crosstalk Between Hepatocyte E4BP4 and Hepatic Stellate Cells Promotes MASH-Associated Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Understanding the complex macrophage landscape in MASLD.JHEP reports : innovation in hepatology · 2024Review
- Hepatic stearoyl-CoA desaturase-1 deficiency induces fibrosis and hepatocellular carcinoma-related gene activation under a high carbohydrate low fat diet.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024Article
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issuedCorrection:2020
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveLiver fibrosis is associated with significant collagen-I deposition largely produced by activated hepatic stellate cells (HSCs); yet, the link between hepatocyte damage and the HSC profibrogenic response remains unclear. Here we show significant induction of osteopontin (OPN) and high-mobility group box-1 (HMGB1) in liver fibrosis. Since OPN was identified as upstream of HMGB1, we hypothesised that OPN could participate in the pathogenesis of liver fibrosis by increasing HMGB1 to upregulate collagen-I expression. DESIGN AND
resultsPatients with long-term hepatitis C virus (HCV) progressing in disease stage displayed enhanced hepatic OPN and HMGB1 immunostaining, which correlated with fibrosis stage, whereas it remained similar in non-progressors. Hepatocyte cytoplasmic OPN and HMGB1 expression was significant while loss of nuclear HMGB1 occurred in patients with HCV-induced fibrosis compared with healthy explants. Well-established liver fibrosis along with marked induction of HMGB1 occurred in CCl
conclusionsDuring liver fibrosis, the increase in OPN induces HMGB1, which acts as a downstream alarmin driving collagen-I synthesis in HSCs.
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What OpenQuestion holds
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.