ArticleThe Journal of clinical investigation2018
HMGB1 promotes ductular reaction and tumorigenesis in autophagy-deficient livers.
Article 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 It has been retracted, and should not be counted.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 69 papers, 1 of them a synthesis that pooled it.
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
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- HMGB1 links chronic liver injury to progenitor responses and hepatocarcinogenesis.The Journal of clinical investigation · 2018Trial
- Dual Immune Lineage Activation Underlies Systemic Immunopathology in Acute-on-Chronic Liver Failure.The American journal of pathology · 2026Article
- Overlapping Yet Distinct Functions of Vacuole Membrane Protein 1 and Transmembrane Protein 41B in Modulating Hepatic Lipoprotein Secretion and Autophagy.Cellular and molecular gastroenterology and hepatology · 2026Article
- Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025Review
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- Transcriptional changes impact hepatic proteome in autophagy-impaired liver.FEBS open bio · 2024Article
- Gfi-1 modulates HMGB1-Mediated autophagy to overcome oxaliplatin resistance in colorectal cancer.Heliyon · 2024Article
- Unraveling the complexities of fibrosis and ductular reaction in liver disease: pathogenesis, mechanisms, and therapeutic insights.American journal of physiology. Cell physiology · 2024Review
- Autophagy and Senescence: The Molecular Mechanisms and Implications in Liver Diseases.International journal of molecular sciences · 2023Review
- NRF2 transcriptionally regulates Caspase-11 expression to activate HMGB1 release by Autophagy-deficient hepatocytes.Cell death discovery · 2023Article
- The Triterpenoid Nrf2 Activator, CDDO-Me, Decreases Neutrophil Senescence in a Murine Model of Joint Damage.International journal of molecular sciences · 2023Article
- Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy.Biomedicines · 2023Review
- Regulatory mechanisms of HMGB1 and its receptors in polycystic ovary syndrome-driven gravid uterine inflammation.The FEBS journal · 2023Article
- Impaired hepatic autophagy exacerbates hepatotoxin induced liver injury.Cell death discovery · 2023Article
- Babao Dan decreases hepatocarcinogenesis by inhibiting hepatic progenitor cells malignant transformation via down-regulating toll-like receptor 4.Frontiers in oncology · 2023Article
- Mechanism of exosomes in the tumor microenvironment in the abscopal effect (Review).International journal of oncology · 2023Article
- The Tumor Microenvironment of Hepatocellular Carcinoma: Untying an Intricate Immunological Network.Cancers · 2022Review
- HMGB1 induces radioresistance through PI3K/AKT/ATM pathway in esophageal squamous cell carcinoma.Molecular biology reports · 2022Article
- Reappraisal of oxidized HMGB1 as a mediator and biomarker.Future science OA · 2022Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
- Correction · 2019-05-02Concerns/Issues about Authorship/Affiliation · Concerns/Issues about Data · Concerns/Issues about Image · Upgrade/Update of Prior Notice(s) · · see https://www.jci.org/articles/view/91814; Daniel J Antione removed from author list;
- Expression of concern · 2019-05-01Concerns/Issues about Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author ·
- Erratum issued
- Expression of concern
Authors and funding
13 authors at 8 institutions in 5 countries.
Funding
Abstract
Autophagy is important for liver homeostasis, and the deficiency leads to injury, inflammation, ductular reaction (DR), fibrosis, and tumorigenesis. It is not clear how these events are mechanistically linked to autophagy deficiency. Here, we reveal the role of high-mobility group box 1 (HMGB1) in two of these processes. First, HMGB1 was required for DR, which represents the expansion of hepatic progenitor cells (HPCs) implicated in liver repair and regeneration. DR caused by hepatotoxic diets (3,5-diethoxycarbonyl-1,4-dihydrocollidine [DDC] or choline-deficient, ethionine-supplemented [CDE]) also depended on HMGB1, indicating that HMGB1 may be generally required for DR in various injury scenarios. Second, HMGB1 promoted tumor progression in autophagy-deficient livers. Receptor for advanced glycation end product (RAGE), a receptor for HMGB1, was required in the same two processes and could mediate the proliferative effects of HMBG1 in isolated HPCs. HMGB1 was released from autophagy-deficient hepatocytes independently of cellular injury but depended on NRF2 and the inflammasome, which was activated by NRF2. Pharmacological or genetic activation of NRF2 alone, without disabling autophagy or causing injury, was sufficient to cause inflammasome-dependent HMGB1 release. In conclusion, HMGB1 release is a critical mechanism in hepatic pathogenesis under autophagy-deficient conditions and leads to HPC expansion as well as tumor progression.
Indexed as
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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.