ArticleJCI insight2024
The STAT3/SETDB2 axis dictates NF-κB-mediated inflammation in macrophages during wound repair.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosomes orchestrate immune homeostasis in acute ischemia-reperfusion flap injury and chronic wounds: the TLR4/NF-κB-STAT3 R-ratio balance decision model, engineering optimization and translational clinical strategy.Frontiers in immunology · 2026Pooled it
- Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations.Journal of cellular and molecular medicine · 2026Review
- Parthenolide accelerates diabetic wound healing through the STAT3 and TNF-α/NF-kappaB pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Therapeutic implications of epigenetic alterations in burns: a new frontier in burn medicine.Clinical science (London, England : 1979) · 2026Review
- Integrated analysis of differential m6A methylation and transcriptome profiles in ovaries of young and aged Qira black sheep.BMC genomics · 2026Article
- SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Long non-coding RNAs as molecular links and circulating biomarkers between type 2 diabetes and colorectal cancer: focus on shared signaling pathways, epigenetic regulation, and ubiquitination mechanisms.Frontiers in molecular biosciences · 2026Review
- Reprogramming the wound microenvironment: identity remodeling strategies for fibroblasts, keratinocytes, and macrophages.Frontiers in immunology · 2026Review
- CD73-Overexpressing ADSCs Promote Neurogenic Bladder Repair via A2A-JAK1/STAT3-Mediated Modulation of Inflammation and Macrophage Polarization.Stem cells international · 2026Article
- Apigenin ameliorates postoperative inflammation and accelerates wound healing in a rat model of perianal abscess by targeting the JAK1/STAT3 pathway in macrophages.Frontiers in immunology · 2026Article
- Liquiritin restores metabolic homeostasis in NAFLD by modulating AKT1/FOXO1 signaling.Frontiers in pharmacology · 2026Article
- Productivity of National Cancer Institute K Awardees and Their Transition to Independent Funding.Journal of cancer education : the official journal of the American Association for Cancer Education · 2025Article
- TNF-α represses fibroblast to myofibroblast transition through the histone methyltransferase Setdb2.JCI insight · 2025Article
- Unraveling the Mechanisms of Madecassoside Derivatives in Wound Healing: Network Pharmacology and Experimental Validation.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Mechanisms of Impaired Wound Healing in Type 2 Diabetes: The Role of Epigenetic Factors.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Macrophage transition from an inflammatory to reparative phenotype after tissue injury is controlled by epigenetic enzymes that regulate inflammatory gene expression. We have previously identified that the histone methyltransferase SETDB2 in macrophages drives tissue repair by repressing NF-κB-mediated inflammation. Complementary ATAC-Seq and RNA-Seq of wound macrophages isolated from mice deficient in SETDB2 in myeloid cells revealed that SETDB2 suppresses the inflammatory gene program by inhibiting chromatin accessibility at NF-κB-dependent gene promoters. We found that STAT3 was required for SETDB2 expression in macrophages, yet paradoxically, it also functioned as a binding partner of SETDB2 where it repressed SETDB2 activity by inhibiting its interaction with the NF-κB component, RELA, leading to increased RELA/NF-κB-mediated inflammatory gene expression. Furthermore, RNA-Seq in wound macrophages from STAT3-deficient mice corroborated this and revealed STAT3 and SETDB2 transcriptionally coregulate overlapping genes. Finally, in diabetic wound macrophages, STAT3 expression and STAT3/SETDB2 binding were increased. We have identified what we believe to be a novel STAT3/SETDB2 axis that modulates macrophage phenotype during tissue repair and may be an important therapeutic target for nonhealing diabetic wounds.
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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.