ArticleParticle and fibre toxicology2024
Macrophage-derived exosomal HMGB3 regulates silica-induced pulmonary inflammation by promoting M1 macrophage polarization and recruitment.
Article in Particle and fibre toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- How extracellular vesicles contribute to pulmonary fibrosis: miRNA-mediated mechanisms, diagnostic potential, and emerging therapeutic strategies.Molecular biology reports · 2026Review
- Review
- Integrative analysis of HMGB3 in esophageal carcinoma: expression profile, prognostic significance, and immune microenvironment associations.Translational cancer research · 2026Article
- HMGB3: A pivotal orchestrator of therapy resistance and cancer stemness in human malignancies (Review).Oncology reports · 2026Review
- SPP1+ Macrophages and the Orchestration of Spatially Organized Immunosuppression in Cancer.Biomedicines · 2026Review
- The mechanism of indigo naturalis and its active ingredients against ulcerative colitis.Scientific reports · 2026Article
- Serum HMGB3 and PCSK9 Levels as Predictors of Early Treatment Response in PediatricInternational journal of general medicine · 2026Article
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- [Risk Factors and Prognosis of Pneumoconiosis Combined With Bacterial Pneumonia: Application of a Random Forest Model].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Hsa_circ_0004662 Accelerates the Progression of Ulcerative Colitis via the microRNA-532/HMGB3 Signalling Axis.Journal of cellular and molecular medicine · 2025Article
- Biomimetic ECM nerve guidance conduit with dynamic 3D interconnected porous network and sustained IGF-1 delivery for enhanced peripheral nerve regeneration and immune modulation.Materials today. Bio · 2025Article
- Long COVID in Elderly COPD Patients: Clinical Features, Pulmonary Function Decline, and Proteomic Insights.International journal of chronic obstructive pulmonary disease · 2025Article
- Development of a machine learning-based risk prediction model for early-stage pneumoconiosis: a retrospective study.Frontiers in medicine · 2025Article
- Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic inflammation and fibrosis are characteristics of silicosis, and the inflammatory mediators involved in silicosis have not been fully elucidated. Recently, macrophage-derived exosomes have been reported to be inflammatory modulators, but their role in silicosis has not been explored. The purpose of the present study was to investigate the role of macrophage-derived exosomal high mobility group box 3 (HMGB3) in silica-induced pulmonary inflammation.
methodsThe induction of the inflammatory response and the recruitment of monocytes/macrophages were evaluated by immunofluorescence, flow cytometry and transwell assays. The expression of inflammatory cytokines was examined by RT-PCR and ELISA, and the signalling pathways involved were examined by western blot analysis.
resultsHMGB3 expression was increased in exosomes derived from silica-exposed macrophages. Exosomal HMGB3 significantly upregulated the expression of inflammatory cytokines, activated the STAT3/MAPK (ERK1/2 and p38)/NF-κB pathways in monocytes/macrophages, and promoted the migration of these cells by CCR2.
conclusionsExosomal HMGB3 is a proinflammatory modulator of silica-induced inflammation that promotes the inflammatory response and recruitment of monocytes/macrophages by regulating the activation of the STAT3/MAPK/NF-κB/CCR2 pathways.
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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 Socratic graph.