ArticleMediators of inflammation2013
HMGB1 acts in synergy with lipopolysaccharide in activating rheumatoid synovial fibroblasts via p38 MAPK and NF-κB signaling pathways.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Meta-Analysis of Methamphetamine Modulation on Amyloid Precursor Protein through HMGB1 in Alzheimer's Disease.International journal of molecular sciences · 2021Pooled it
- Serial assessment of serum HMGB1 and ΔSOFA for predicting 28-day mortality in sepsis patients: a prospective cohort study in the emergency department.BMC emergency medicine · 2026Article
- HMGB1 as an emerging key modulator of bone remodeling: a narrative review.Stem cell research & therapy · 2025Review
- Establishment and comparison of human term placenta-derived trophoblast cells†.Biology of reproduction · 2024Article
- The Role of Alarmins in the Pathogenesis of Rheumatoid Arthritis, Osteoarthritis, and Psoriasis.Current issues in molecular biology · 2024Review
- Demonstration of ameliorating effect of papaverine in sepsis-induced acute lung injury on rat model through radiology and histology.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2023Article
- The mechanism of action of paeoniae radix rubra-angelicae sinensis radix drug pair in the treatment of rheumatoid arthritis through PI3K/AKT/NF-κB signaling pathway.Frontiers in pharmacology · 2023Article
- Extracellular HMGB1 as Inflammatory Mediator in the Progression of Mycoplasma Gallisepticum Infection.Cells · 2022Article
- AGE/Non-AGE Glycation: An Important Event in Rheumatoid Arthritis Pathophysiology.Inflammation · 2022Review
- HMGB1: A Potential Target of Nervus Vagus Stimulation in Pediatric SARS-CoV-2-Induced ALI/ARDS.Frontiers in pediatrics · 2022Article
- Lipopolysaccharides induce a RAGE-mediated sensitization of sensory neurons and fluid hypersecretion in the upper airways.Scientific reports · 2021Article
- The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach.Life sciences · 2020Review
- Glycyrrhizin Inhibits PEDV Infection and Proinflammatory Cytokine Secretion via the HMGB1/TLR4-MAPK p38 Pathway.International journal of molecular sciences · 2020Article
- HMGB1/PI3K/Akt/mTOR Signaling Participates in the Pathological Process of Acute Lung Injury by Regulating the Maturation and Function of Dendritic Cells.Frontiers in immunology · 2020Article
- High-mobility group box1 as an amplifier of immune response and target for treatment inInternational journal of ophthalmology · 2020Article
- High-Mobility Group Box 1 (HMGB1) and Autophagy in Acute Lung Injury (ALI): A Review.Medical science monitor : international medical journal of experimental and clinical research · 2019Review
- Johnny on the Spot-Chronic Inflammation Is Driven by HMGB1.Frontiers in immunology · 2019Review
- Propofol protects against endotoxin-induced myocardial injury by inhibiting NF-κB-mediated inflammation.Experimental and therapeutic medicine · 2018Article
- High mobility group box protein 1 downregulates acid β-glucosidase 1 in synovial fibroblasts from patients with rheumatoid arthritis.International journal of clinical and experimental pathology · 2018Article
- Trauma-Induced Damage-Associated Molecular Patterns-Mediated Remote Organ Injury and Immunosuppression in the Acutely Ill Patient.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synovial fibroblasts (SF) play a central role in the inflammatory and destructive process in rheumatoid arthritis (RA). High-mobility group box chromosomal protein 1 (HMGB1) or lipopolysaccharide (LPS) alone failed to induce significant changes in proliferation of cultured SF from RA patients, but premixed HMGB1 with LPS (HMGB1-LPS) significantly facilitated SF proliferation. HMGB1 alone failed to induce IL-6, MMP-3, and MMP-13 production in cultured SF but greatly enhanced LPS-induced expression of IL-6, MMP-3, and MMP-13 at both mRNA and protein levels. HMGB1-LPS synergistically upregulated TLR4 and receptor for advanced glycation endproducts (RAGE) expression on the surface of SF. Both blockers of TLR4 and RAGE significantly inhibited the synergistic effects of HMGB1-LPS on the production of IL-6 and MMPs, but blocking antibodies to TLR2 failed. HMGB1-LPS synergistically increased intracellular levels of phosphorylated p38 and phosphorylated I κ B. Furthermore, both NF- κ B inhibitor Bay11-7085 and p38 inhibitor SB203580 significantly suppressed the enhanced production of IL-6 and MMPs induced by HMGB1-LPS. In conclusion, HMGB1 acts in synergy with LPS to upregulate TLR4 and RAGE expression on the surface of SF in RA and then to augment IL-6, MMP-3, and MMP-13 production, which depends on p38 MAPK and NF-κB activation.
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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.