ArticleThe EMBO journal2007
A novel pathway of HMGB1-mediated inflammatory cell recruitment that requires Mac-1-integrin.
Article in The EMBO journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 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.
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Who cites it
182 citing papers in PubMed, 373 citations in OpenAlex.
- RAGE controls leukocyte adhesion in preterm and term infants.BMC immunology · 2014Trial
- Real-time kinetics of high-mobility group box 1 (HMGB1) oxidation in extracellular fluids studied by in situ protein NMR spectroscopy.The Journal of biological chemistry · 2013Trial
- Review
- 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
- RAGE Signalling in Acute Inflammatory Disorders: Therapeutic Potential of Natural Products.Biomolecules · 2026Review
- uPAR/suPAR Signaling and Organ Crosstalk in Cardiovascular-Kidney-Metabolic Syndrome.Circulation research · 2026Review
- RAGE in Neutrophils: A Sensor for Pathogen-Associated Structures and Beyond.Biomedicines · 2026Article
- Picropodophyllotoxin Mitigates Severe Inflammation Through HMGB1 Inhibition.Biomolecules · 2026Article
- The Role of the HMGB1 C-Terminal Domain in Epithelial-Mesenchymal Transition and Invasion in 2D and 3D MDA-MB-231 Breast Cancer Models.International journal of molecular sciences · 2026Article
- PANoptosis in diabetes: immunometabolic insights and treatments.Apoptosis : an international journal on programmed cell death · 2026Review
- Extracellular vesicles: biogenesis mechanism and impacts on tumor immune microenvironment.Journal of biomedical science · 2025Review
- Inhibition of SLC25A10 promotes cellular senescence and impedes hepatocellular carcinoma progression.Translational cancer research · 2025Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- 3-Deoxysappanchalcone Inhibited High Mobility Group Box Protein 1-Mediated Severe Inflammatory Responses.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Targeting high-mobility-group-box-1-mediated inflammation: a promising therapeutic approach for myocardial infarction.Inflammopharmacology · 2025Review
- Leukocyte recruitment in flavivirus-induced encephalitis.Frontiers in immunology · 2025Review
- DAMP-driven trained immunity: metabolic and epigenetic reprogramming in critical illness and chronic inflammation.Frontiers in immunology · 2025Review
- Platelets as central hubs of inflammation.Frontiers in immunology · 2025Review
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
122 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
11 authors at 6 institutions in 4 countries.
Funding
Abstract
High-mobility group box 1 (HMGB1) is released extracellularly upon cell necrosis acting as a mediator in tissue injury and inflammation. However, the molecular mechanisms for the proinflammatory effect of HMGB1 are poorly understood. Here, we define a novel function of HMGB1 in promoting Mac-1-dependent neutrophil recruitment. HMGB1 administration induced rapid neutrophil recruitment in vivo. HMGB1-mediated recruitment was prevented in mice deficient in the beta2-integrin Mac-1 but not in those deficient in LFA-1. As observed by bone marrow chimera experiments, Mac-1-dependent neutrophil recruitment induced by HMGB1 required the presence of receptor for advanced glycation end products (RAGE) on neutrophils but not on endothelial cells. In vitro, HMGB1 enhanced the interaction between Mac-1 and RAGE. Consistently, HMGB1 activated Mac-1 as well as Mac-1-mediated adhesive and migratory functions of neutrophils in a RAGE-dependent manner. Moreover, HMGB1-induced activation of nuclear factor-kappaB in neutrophils required both Mac-1 and RAGE. Together, a novel HMGB1-dependent pathway for inflammatory cell recruitment and activation that requires the functional interplay between Mac-1 and RAGE is described here.
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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.