ArticlePloS one2013
High-mobility group box 1 inhibits gastric ulcer healing through Toll-like receptor 4 and receptor for advanced glycation end products.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Enhanced Therapeutic Efficacy of Omeprazole Nanosuspension in Ethanol-Induced Gastric Ulcer: A Focus on Oxidative Stress and Inflammatory Pathways.Biomolecules · 2025Article
- Article
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- Combined effect of pantoprazole and mesenchymal stem cells on experimentally induced gastric ulcer: implication of oxidative stress, inflammation and apoptosis pathways.Inflammopharmacology · 2024Article
- Amelioration of ethanol-induced gastric ulcer in rats by quercetin: implication of Nrf2/HO1 and HMGB1/TLR4/NF-κB pathways.Heliyon · 2022Article
- Opioid Use in Murine Model Results in Severe Gastric Pathology that May Be Attenuated by Proton Pump Inhibition.The American journal of pathology · 2022Article
- Gastric alarmin release: A warning signal in the development of gastric mucosal diseases.Frontiers in immunology · 2022Review
- Time to Develop Therapeutic Antibodies Against Harmless Proteins Colluding with Sepsis Mediators?ImmunoTargets and therapy · 2020Review
- Gastric acid inhibitor aggravates indomethacin-induced small intestinal injury via reducing Lactobacillus johnsonii.Scientific reports · 2019Article
- Article
- Increased HMGB1 expression correlates with higher expression of c-IAP2 and pERK in colorectal cancer.Medicine · 2019Article
- Microbiome and intestinal ischemia/reperfusion injury.Journal of clinical biochemistry and nutrition · 2018Review
- Necrostatin-1 Attenuates Trauma-Induced Mouse Osteoarthritis and IL-1β Induced Apoptosis via HMGB1/TLR4/SDF-1 in Primary Mouse Chondrocytes.Frontiers in pharmacology · 2018Article
- Necrostatin-1 Protects Against D-Galactosamine and Lipopolysaccharide-Induced Hepatic Injury by Preventing TLR4 and RAGE Signaling.Inflammation · 2017Article
- Nutritional Aspects of Gastrointestinal Wound Healing.Advances in wound care · 2016Review
- HMGB1 promotes HCC progression partly by downregulating p21 via ERK/c-Myc pathway and upregulating MMP-2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Ionizing Radiation Induces HMGB1 Cytoplasmic Translocation and Extracellular Release.Guo ji fang she yi xue he yi xue za zhi = International journal of radiation medicine and nuclear medicine · 2016Article
- rhHMGB1 drives osteoblast migration in a TLR2/TLR4- and NF-κB-dependent manner.Bioscience reports · 2016Article
- High Mobility Group Box-1 Promotes Inflammation-Induced Lymphangiogenesis via Toll-Like Receptor 4-Dependent Signalling Pathway.PloS one · 2016Article
- Emerging Targets for Therapeutic Development in Diabetes and Its Complications: The RAGE Signaling Pathway.Clinical pharmacology and therapeutics · 2015Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group box 1 (HMGB1) was initially discovered as a nuclear protein that interacts with DNA as a chromatin-associated non-histone protein to stabilize nucleosomes and to regulate the transcription of many genes in the nucleus. Once leaked or actively secreted into the extracellular environment, HMGB1 activates inflammatory pathways by stimulating multiple receptors, including Toll-like receptor (TLR) 2, TLR4, and receptor for advanced glycation end products (RAGE), leading to tissue injury. Although HMGB1's ability to induce inflammation has been well documented, no studies have examined the role of HMGB1 in wound healing in the gastrointestinal field. The aim of this study was to evaluate the role of HMGB1 and its receptors in the healing of gastric ulcers. We also investigated which receptor among TLR2, TLR4, or RAGE mediates HMGB1's effects on ulcer healing. Gastric ulcers were induced by serosal application of acetic acid in mice, and gastric tissues were processed for further evaluation. The induction of ulcer increased the immunohistochemical staining of cytoplasmic HMGB1 and elevated serum HMGB1 levels. Ulcer size, myeloperoxidase (MPO) activity, and the expression of tumor necrosis factor α (TNFα) mRNA peaked on day 4. Intraperitoneal administration of HMGB1 delayed ulcer healing and elevated MPO activity and TNFα expression. In contrast, administration of anti-HMGB1 antibody promoted ulcer healing and reduced MPO activity and TNFα expression. TLR4 and RAGE deficiency enhanced ulcer healing and reduced the level of TNFα, whereas ulcer healing in TLR2 knockout (KO) mice was similar to that in wild-type mice. In TLR4 KO and RAGE KO mice, exogenous HMGB1 did not affect ulcer healing and TNFα expression. Thus, we showed that HMGB1 is a complicating factor in the gastric ulcer healing process, which acts through TLR4 and RAGE to induce excessive inflammatory responses.
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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.