Trial reportThe Journal of clinical investigation2018
HMGB1 links chronic liver injury to progenitor responses and hepatocarcinogenesis.
Trial report in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 67 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
67 citing papers in PubMed, 112 citations in OpenAlex.
- Advances in pharmacological interventions for hepatic fibrosis: from pathogenic mechanisms to novel therapeutic targets.Annals of medicine · 2026Review
- Ischemic preconditioning promotes hepatic differentiation in human liver organoids.Frontiers in cell and developmental biology · 2026Article
- Natural products as therapeutic interventions for inflammation-mediated cancer.Discover oncology · 2025Review
- Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells.Cellular & molecular immunology · 2025Review
- Impact of Clonorchis sinensis infection on long-term survival after curative resection for hepatocellular carcinoma: A multicenter cohort study.PLoS neglected tropical diseases · 2025Article
- High Mobility Group Box 1 Is Potential Target Therapy for Inhibiting Metastasis and Enhancing Drug Sensitivity of Hepatocellular Carcinoma.International journal of molecular sciences · 2025Article
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- HMGB1/TREM1 crosstalk between heat-injured hepatocytes and macrophages promotes HCC progression after RFA.Journal of cancer research and clinical oncology · 2024Article
- Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression.Signal transduction and targeted therapy · 2024Article
- HMGB1-Mediated Cell Death-A Crucial Element in Post-Hepatectomy Liver Failure.International journal of molecular sciences · 2024Article
- Immune Cell Migration to Cancer.Cells · 2024Review
- PARD3 drives tumorigenesis through activating Sonic Hedgehog signalling in tumour-initiating cells in liver cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- NcRNA Regulated Pyroptosis in Liver Diseases and Traditional Chinese Medicine Intervention: A Narrative Review.Journal of inflammation research · 2024Review
- Molecular Biological Mechanisms of Action of Chrysophanol in Hepatic Stellate Cells Activated by Hepatic B Virus X Based on Network Pharmacology.Intervirology · 2024Article
- The multifunctional protein HMGB1: 50 years of discovery.Nature reviews. Immunology · 2023Review
- Transcription factor E4F1 as a regulator of cell life and disease progression.Science advances · 2023Review
- Adenosine A2A receptor is a tumor suppressor of NASH-associated hepatocellular carcinoma.Cell reports. Medicine · 2023Article
- Mechanisms involved in the HMGB1 modulation of tumor multidrug resistance (Review).International journal of molecular medicine · 2023Article
- NRF2 transcriptionally regulates Caspase-11 expression to activate HMGB1 release by Autophagy-deficient hepatocytes.Cell death discovery · 2023Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern · 2019-03-31Falsification/Fabrication of Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · Daniel J Antoine removed from author list;
- Correction · 2019-04-01Error in Image · Falsification/Fabrication of Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Retract and Replace · · Daniel J Antoine removed from author list;
- Erratum issued
- Expression of concern
Authors and funding
6 authors at 4 institutions in 4 countries.
Funding
Abstract
Cell death is a key driver of disease progression and carcinogenesis in chronic liver disease (CLD), highlighted by the well-established clinical correlation between hepatocellular death and risk for the development of cirrhosis and hepatocellular carcinoma (HCC). Moreover, hepatocellular death is sufficient to trigger fibrosis and HCC in mice. However, the pathways through which cell death drives CLD progression remain elusive. Here, we tested the hypothesis that high-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) with key roles in acute liver injury, may link cell death to injury responses and hepatocarcinogenesis in CLD. While liver-specific HMGB1 deficiency did not significantly affect chronic injury responses such as fibrosis, regeneration, and inflammation, it inhibited ductular/progenitor cell expansion and hepatocyte metaplasia. HMGB1 promoted ductular expansion independently of active secretion in a nonautonomous fashion, consistent with its role as a DAMP. Liver-specific HMGB1 deficiency reduced HCC development in 3 mouse models of chronic injury but not in a model lacking chronic liver injury. As with CLD, HMGB1 ablation reduced the expression of progenitor and oncofetal markers, a key determinant of HCC aggressiveness, in tumors. In summary, HMGB1 links hepatocyte death to ductular reaction, progenitor signature, and hepatocarcinogenesis in CLD.
Indexed as
Identifiers
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.