ArticleDiabetes2024
Diabetic Wound Keratinocytes Induce Macrophage JMJD3-Mediated Nlrp3 Expression via IL-1R Signaling.
Article in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed.
- Inflammasome-derived biomarkers in wound healing: linking tissue repair, chronic inflammation, fibrosis, and precision therapeutics.Molecular biology reports · 2026Review
- Preclinical Efficacy of Recombinant Human Platelet-Derived Growth Factor-BB in Experimental Diabetic Wound Healing: A Systematic Review and Meta-Analysis of Animal Studies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations.Journal of cellular and molecular medicine · 2026Review
- Fibroblasts resistScience advances · 2026Article
- Schwann cell derived extracellular vesicles are multifunctional nanotherapeutic mediators for diabetic oral mucosal wound healing.Discover nano · 2026Review
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Epigenetic regulation of PANoptosis: DNA methylation, histone modifications and non-coding RNAs.EXCLI journal · 2026Review
- Exosome-Biomaterial Platforms for Diabetic Skin Infections: Microenvironment Remodeling, Responsive Delivery, and Clinical Translation.International journal of nanomedicine · 2026Review
- Spatiotemporal regulation of acute wound healing by the NLRP3 inflammasome: dual roles in macrophage-fibroblast chemotaxis and phenotype during wound repair.Burns & trauma · 2026Article
- Single-cell RNA sequencing in diabetic foot ulcers: pathogenesis, biomarkers, and translational potential.Frontiers in clinical diabetes and healthcare · 2026Review
- M2 macrophage-derived extracellular vesicle/polydopamine hydrogel attenuates diabetic periodontitis-induced bone loss via the NEK7/NLRP3/IL-1β pathway.Scientific reports · 2025Article
- IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3.Nature communications · 2025Article
- AhR deficiency exacerbates inflammation in diabetic wounds via impaired mitophagy and cGAS-STING-NLRP3 activation: Therapeutic potential of hydrogels loaded with FICZ.Materials today. Bio · 2025Article
- Pyroptosis-responsive microspheres modulate the inflammatory microenvironment to retard osteoporosis in female mice.Nature communications · 2025Article
- The Impact of PCSK9 on Diabetic Cardiomyopathy: Mechanisms and Implications.Biomolecules · 2025Review
- Mechanisms of Impaired Wound Healing in Type 2 Diabetes: The Role of Epigenetic Factors.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Macrophage polarization: molecular mechanisms, disease implications, and targeted therapeutic strategies.Frontiers in immunology · 2025Review
- Disulfiram-loaded nanovesicles hydrogel promotes healing of diabetic wound.Journal of translational medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Macrophage (Mφ) plasticity is critical for normal wound repair; however, in type 2 diabetic wounds, Mφs persist in a low-grade inflammatory state that prevents the resolution of wound inflammation. Increased NLRP3 inflammasome activity has been shown in diabetic wound Mφs; however, the molecular mechanisms regulating NLRP3 expression and activity are unclear. Here, we identified that diabetic wound keratinocytes induce Nlrp3 gene expression in wound Mφs through IL-1 receptor-mediated signaling, resulting in enhanced inflammasome activation in the presence of pathogen-associated molecular patterns and damage-associated molecular patterns. We found that IL-1α is increased in human and murine wound diabetic keratinocytes compared with nondiabetic controls and directly induces Mφ Nlrp3 expression through IL-1 receptor signaling. Mechanistically, we report that the histone demethylase, JMJD3, is increased in wound Mφs late post-injury and is induced by IL-1α from diabetic wound keratinocytes, resulting in Nlrp3 transcriptional activation through an H3K27me3-mediated mechanism. Using genetically engineered mice deficient in JMJD3 in myeloid cells (Jmjd3f/flyz2Cre+), we demonstrate that JMJD3 controls Mφ-mediated Nlrp3 expression during diabetic wound healing. Thus, our data suggest a role for keratinocyte-mediated IL-1α/IL-1R signaling in driving enhanced NLRP3 inflammasome activity in wound Mφs. These data also highlight the importance of cell cross-talk in wound tissues and identify JMJD3 and the IL-1R signaling cascade as important upstream therapeutic targets for Mφ NLRP3 inflammasome hyperactivity in nonhealing diabetic wounds. ARTICLE HIGHLIGHTS:
Indexed as
Identifiers
What OpenQuestion holds
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.