ArticleCellular & molecular immunology2015
HMGB1 contributes to allergen-induced airway remodeling in a murine model of chronic asthma by modulating airway inflammation and activating lung fibroblasts.
Article in Cellular & molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 84 citations in OpenAlex.
- Differential DAMP release was observed in the sputum of COPD, asthma and asthma-COPD overlap (ACO) patients.Scientific reports · 2019Trial
- HMGB1 Upregulates MMP-1-Mediated Mesothelial-Mesenchymal Transition and Promotes Pleural Fibrosis in Tuberculous Pleural Effusion.International journal of molecular sciences · 2026Article
- HMGB1 promotes intracranial aneurysm progression by regulating vascular smooth muscle cell phenotypic switching and ferroptosis.Journal of molecular histology · 2026Article
- Obesity and respiratory diseases: mechanisms, phenotypes, and clinical implications.Diabetology & metabolic syndrome · 2026Review
- The Role of Alarmins in the Pathogenesis of Asthma.Biomolecules · 2025Review
- The Effects of Obesity on Lung Physiology, the Prevalence and Severity of Chronic Pulmonary Diseases, and Inhalation Treatment.Drug design, development and therapy · 2025Review
- Mechanism of miR-130b-3p in relieving airway inflammation in asthma through HMGB1-TLR4-DRP1 axis.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Regulation of Airway Epithelial-Derived Alarmins in Asthma: Perspectives for Therapeutic Targets.Biomedicines · 2024Review
- HMGB1 derived from lung epithelial cells after cobalt nanoparticle exposure promotes the activation of lung fibroblasts.Nanotoxicology · 2024Article
- Inhibition of xanthine oxidase by allopurinol suppresses HMGB1 secretion and ameliorates experimental asthma.Redox biology · 2024Article
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.Frontiers in allergy · 2024Review
- HMGB1/RAGE Signaling Regulates Th17/IL-17 and Its Role in Bronchial Epithelial-Mesenchymal Transformation.Current molecular medicine · 2024Article
- In-silico identification and prioritization of therapeutic targets of asthma.Scientific reports · 2023Article
- CXCL12/CXCR4 Axis is Involved in the Recruitment of NK Cells by HMGB1 Contributing to Persistent Airway Inflammation and AHR During the Late Stage of RSV Infection.Journal of microbiology (Seoul, Korea) · 2023Article
- Anti-S100A4 antibody administration alleviates bronchial epithelial-mesenchymal transition in asthmatic mice.Open medicine (Warsaw, Poland) · 2023Article
- Epithelial microRNA-30a-3p targets RUNX2/HMGB1 axis to suppress airway eosinophilic inflammation in asthma.Respiratory research · 2022Article
- Airway epithelial cell-specific deletion of HMGB1 exaggerates inflammatory responses in mice with muco-obstructive airway disease.Frontiers in immunology · 2022Article
- Predictive value of S100A4 in eosinophilic chronic rhinosinusitis with nasal polyps.Frontiers in surgery · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pro-inflammation factor high-mobility group box protein 1 (HMGB1) has been implicated in the pathogenesis of asthma. In this study, we used a murine model of chronic asthma to evaluate the effects of HMGB1 on airway remodeling. Female BALB/c mice were randomly divided into four groups: control, ovalbumin (OVA) asthmatic, OVA+isotype antibody and OVA+anti-HMGB1 antibody. Anti-HMGB1 antibody therapy was started on day 21 and was administered three times per week for 6 weeks before intranasal challenge with OVA. In this mouse model, HMGB1 expression is significantly elevated. The anti-HMGB1 antibody group exhibited decreased levels of immunoglobulin E (IgE) and inflammatory mediators and reduced inflammatory cell accumulation, airway hyperresponsiveness (AHR), mucus synthesis, smooth muscle thickness and lung collagen content compared with the OVA groups. Treatment with HMGB1 increased proliferation, migration, collagen secretion and α-smooth muscle actin (SMA) expression in MRC-5 cells. Treatment with the HMGB1/IL-1β complex significantly increased the expression and secretion of transforming growth factor (TGF-β1), matrix metalloproteinase (MMP)-9 and vascular endothelial growth factor (VEGF). Altogether, these results suggest that blocking HMGB1 activity may reverse airway remodeling by suppressing airway inflammation and modulating lung fibroblast phenotype and activation.
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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.