ReviewJournal of cellular physiology2021
HMGB1 as a therapeutic target in disease.
Review in Journal of cellular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 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
173 citing papers in PubMed, 283 citations in OpenAlex.
- Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026Review
- HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Review
- HMGB1 impairs nasal epithelial barrier via regulating autophagy in the pathogenesis of allergic rhinitis.The World Allergy Organization journal · 2026Article
- Revealing the Biological Effect of theJournal of the American Chemical Society · 2026Article
- Article
- HMGB1 promotes intracranial aneurysm progression by regulating vascular smooth muscle cell phenotypic switching and ferroptosis.Journal of molecular histology · 2026Article
- Targeting Immune Dysregulation After Burn Injury for Improved Healing and Outcomes.Biomolecules · 2026Review
- Non-coding RNAs as master regulators of ferroptosis in cancer: mechanisms and clinical implications.Molecular cancer · 2026Review
- Context-dependent release of HMGB1: cell death mode, cell type and LPS stress drive monomer and heterocomplex formation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4/NF-κB/IL-6/STAT3 Signalling Cascade.Journal of cellular and molecular medicine · 2026Article
- The SMAD-Pathway Mediates HMGB1-Induced Proliferation and Metastatic Progression in Cutaneous Squamous Cell Carcinoma Cells.Annals of dermatology · 2026Article
- Article
- Toll-Like Receptors in Diabetes: Immunometabolic Mechanisms and Emerging Precision Therapeutic Strategies.Journal of inflammation research · 2026Review
- Immediate post-injury HMGB1 neutralization prevents synaptic dysfunction in burn and hindlimb unloaded rats.Frontiers in immunology · 2026Article
- Syringic acid attenuates LPS-induced acute lung injury via modulation of the HMGB1/TLR4/NF-κB and Keap1/Nrf2/HO-1 pathways: Mechanistic insights fromIranian journal of basic medical sciences · 2026Article
- Exploratory evaluation of miR-146, inflammatory biomarkers, and subjective cognitive symptoms in chronic migraine.Turkish journal of medical sciences · 2026Article
- Advances in the Basic Sciences in Thoracic Oncology in the Last 20 Years and Their Translational Impact.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026Review
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- Integrative prognostic model incorporating high mobility group box 1 subcellular localization and tumor-infiltrating lymphocytes in early-stage lung adenocarcinoma.Diagnostic pathology · 2025Article
113 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
High-mobility group box 1 (HMGB1) was initially recognized as a ubiquitous nuclear protein involved in maintaining the nucleosome integrity and facilitating gene transcription. HMGB1 has since been reevaluated to be a prototypical damage-associated molecular pattern (DAMP) protein, and together with its exogenous counterpart, pathogen-associated molecular pattern (PAMP), completes the body's alarmin system against disturbances in homeostasis. HMGB1 can be released into the extracellular matrix (ECM) by either granulocytes or necrotic cells to serve as a chemotaxis/cytokine during infection, endotoxemia, hypoxia, ischemia-reperfusion events, and cancer. Different isoforms of HMGB1 present with distinctive physiological functions in ECM-fully-reduced HMGB1 (all thiol) acts as the initial damage signal to recruit circulating myeloid cells, disulfide HMGB1 behaves as a cytokine to activate macrophages and neutrophils, and both signals are turned off when HMGB1 is terminally oxidized into the final sulfonate form. Targeting HMGB1 constitutes a favorable therapeutic strategy for inflammation and inflammatory diseases. Antagonists such as ethyl pyruvate inhibit HMGB1 by interfering with its cytoplasmic exportation, while others such as glycyrrhizin directly bind to HMGB1 and render it unavailable for its receptors. The fact that a mixture of different HMGB1 isoforms is present in the ECM poses a challenge in pinpointing the exact role of an individual antagonist. A more discriminative probe for HMGB1 may be necessary to advance our knowledge of HMGB1, HMGB1 antagonists, and inflammatory-related diseases.
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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.