ArticleImmunity2019
The Histone Methyltransferase Setdb2 Modulates Macrophage Phenotype and Uric Acid Production in Diabetic Wound Repair.
Article in Immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
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Who cites it
88 citing papers in PubMed, 159 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- MLL1 Regulates T-Cell Phenotype via Notch Signaling During Abdominal Aortic Aneurysm Development.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Parthenolide accelerates diabetic wound healing through the STAT3 and TNF-α/NF-kappaB pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Targeting the cytokine-epigenetic axis: a new paradigm and prospects for disease treatment.European cytokine network · 2026Review
- SETDB2 induces abnormal SHP-1 splicing and promotes immunosuppression in hepatocellular carcinoma.Oncogene · 2026Article
- Engineered polypeptide cascade-release platform restores macrophage plasticity for accelerated diabetic wound healing.Bioactive materials · 2026Article
- SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Adrenergic receptors: a key determinant of outcomes in bacterial pneumonia and bacterial sepsis-associated acute lung injury/acute respiratory distress syndrome through participation in pulmonary innate immune response.Frontiers in immunology · 2026Review
- Protein acetylation in atherosclerosis: beyond inflammation to core cellular processes and therapeutic potential.Frontiers in immunology · 2026Review
- Epigenetic regulation of inflammation by dopamine in primary human macrophages.Frontiers in immunology · 2026Article
- Advances in post-translational and epigenetic modification of hyperuricemia-to-gout progression: mechanisms and therapeutic targets.Frontiers in cell and developmental biology · 2026Review
- Medicinal Plants Facilitate the Recovery of Diabetic Foot Ulcer by Regulating Macrophages: Latest Evidence and Insights.Current diabetes reviews · 2026Review
- Histone post-translational modifications in diabetic foot ulcer healing: linking immune dysregulation to tissue repair.Frontiers in immunology · 2026Review
- Adipose-Derived Stem Cell Exosomes in Diabetic Wound Repair: Molecular Crosstalk, Bioengineering Strategies, and Translational Challenges.Stem cells international · 2026Review
- Clinical severity-dependent virulence ofFrontiers in cellular and infection microbiology · 2026Article
- IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3.Nature communications · 2025Article
- TNF-α represses fibroblast to myofibroblast transition through the histone methyltransferase Setdb2.JCI insight · 2025Article
- Research progress on the role and mechanisms of ferroptosis in diabetic wound repair.Cell death discovery · 2025Review
- Function of epigenetic modifications in wound healing and potential therapies (Review).International journal of molecular medicine · 2025Review
- Review
28 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Macrophage plasticity is critical for normal tissue repair to ensure transition from the inflammatory to the proliferative phase of healing. We examined macrophages isolated from wounds of patients afflicted with diabetes and of healthy controls and found differential expression of the methyltransferase Setdb2. Myeloid-specific deletion of Setdb2 impaired the transition of macrophages from an inflammatory phenotype to a reparative one in normal wound healing. Mechanistically, Setdb2 trimethylated histone 3 at NF-κB binding sites on inflammatory cytokine gene promoters to suppress transcription. Setdb2 expression in wound macrophages was regulated by interferon (IFN) β, and under diabetic conditions, this IFNβ-Setdb2 axis was impaired, leading to a persistent inflammatory macrophage phenotype in diabetic wounds. Setdb2 regulated the expression of xanthine oxidase and thereby the uric acid (UA) pathway of purine catabolism in macrophages, and pharmacologic targeting of Setdb2 or the UA pathway improved healing. Thus, Setdb2 regulates macrophage plasticity during normal and pathologic wound repair and is a target for therapeutic manipulation.
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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.