ArticleCommunications biology2025
Macrophage-derived IL-1β directs fibroblast progenitor cell fate via metabolic reprogramming in wound healing.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Advanced Functional Wound Dressings in Precision Surgery: Immunometabolic Reprogramming, Bioadaptive Biomaterials, and Intelligent Regenerative Interfaces.International journal of molecular sciences · 2026Review
- Inflammaging Beyond Biomarkers: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Cellular and Molecular Mechanisms of Wound Repair: From Biology to Therapeutic Innovation.Cells · 2025Review
- Microbial Biofilms as Barriers to Chronic Wound Healing: Diagnostic Challenges and Therapeutic Advances.Journal of clinical medicine · 2025Review
- Beyond the clot: how the biomolecular landscape of platelet-rich fibrin directs fibroblast functions.Frontiers in oral health · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oral mucosa exhibits unique regenerative properties and distinct wound healing dynamics compared to facial skin, providing a valuable model for studying tissue-specific repair mechanisms. Using a rigorously controlled mouse model combined with single-cell transcriptomics, we identified a novel mechanism underlying this tissue-specific difference. Our study revealed a population of fibroblast progenitors in the oral buccal mucosa that rapidly activate and differentiate into mature fibroblasts, contributing to effective wound resolution. Mechanistically, IL-1β derived from tissue-resident macrophages activates NFκB signals in these progenitors, inducing a metabolic shift from glycolysis to oxidative phosphorylation in a proteasome-dependent manner. This metabolic reprogramming supports stem cell differentiation and contributes to the unique regenerative pattern of the oral buccal mucosa. Our findings highlight the specialized healing mechanisms of the oral tissue and suggest that modulating proteasome activation and the IL-1β/NFκB axis may offer new therapeutic avenues for enhancing wound repair in tissue requiring extensive connective remodeling, such as skin or gingiva.
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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.