ArticleDiabetes2015
Epigenetic changes in bone marrow progenitor cells influence the inflammatory phenotype and alter wound healing in type 2 diabetes.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 2 of them syntheses that pooled it.
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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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Who cites it
128 citing papers in PubMed, 2 syntheses or guidelines pooled it, 199 citations in OpenAlex.
- Skin regenerative potential of hydrogel matrices incorporated with stem cell-derived extracellular vesicles enriched with MicroRNAs: a systematic review.Molecular and cellular biochemistry · 2025Pooled it
- Research progress on the mechanism by which skin macrophage dysfunction mediates chronic inflammatory injury in diabetic skin.Frontiers in endocrinology · 2022Pooled it
- MLL1 Regulates T-Cell Phenotype via Notch Signaling During Abdominal Aortic Aneurysm Development.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Review
- Immune dysregulation in chronic diabetic wounds: therapeutic opportunities for healing reprogramming.Frontiers in immunology · 2026Review
- Combined metabolic stress and nitric oxide synthase inhibition induces tissue-specific remodeling across cardiovascular and hematopoietic compartments during obesity.Frontiers in cardiovascular medicine · 2026Article
- Immune cells in diabetic wound repair: the key to better wound management.Frontiers of medicine · 2025Review
- 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
- Diabetic neuropathy and wound healing: An update on epigenetic crosstalk.World journal of diabetes · 2025Review
- Diet-induced obesity induces oxidative stress and enhances H3K4me3 levels, driving nonresolving inflammation and myelopoiesis in hematopoietic stem and progenitor cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Sodium Alginate Hydrogel Sponges Embedded with M2 Macrophages: An Adoptive Cell Therapy Strategy for Accelerated Diabetic Wound Healing.Gels (Basel, Switzerland) · 2025Article
- Comparing Amniotic Membranes to Other Bioengineered Skin Substitutes in Wound Healing: A Propensity Score-Matched Analysis.Journal of clinical medicine · 2025Article
- Epigenetic alteration of smooth muscle cells regulates endothelin-dependent blood pressure and hypertensive arterial remodeling.The Journal of clinical investigation · 2025Article
- Epigenetic Regulation of Bone Healing: Implications for Fracture Repair and Clinical Treatment Strategies.The Yale journal of biology and medicine · 2025Review
- Progress of microneedle targeted modulation technology in the reconstruction of immune microenvironment in diabetic wounds.European journal of medical research · 2025Review
- Regulation of histone H3K27 methylation in inflammation and cancer.Molecular biomedicine · 2025Review
- Epigenetic regulatory mechanism of macrophage polarization in diabetic wound healing (Review).Molecular medicine reports · 2025Review
- Enrichment of H3S28p and H3K9me2 Epigenetic Marks on Inflammatory-Associated Gene Promoters in Response to Severe Burn Injury.Life (Basel, Switzerland) · 2024Article
- Programmed BRD9 Degradation and Hedgehog Signaling Activation via Silk-Based Core-Shell Microneedles Promote Diabetic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Classically activated (M1) macrophages are known to play a role in the development of chronic inflammation associated with impaired wound healing in type 2 diabetes (T2D); however, the mechanism responsible for the dominant proinflammatory (M1) macrophage phenotype in T2D wounds is unknown. Since epigenetic enzymes can direct macrophage phenotypes, we assessed the role of histone methylation in bone marrow (BM) stem/progenitor cells in the programming of macrophages toward a proinflammatory phenotype. We have found that a repressive histone methylation mark, H3K27me3, is decreased at the promoter of the IL-12 gene in BM progenitors and this epigenetic signature is passed down to wound macrophages in a murine model of glucose intolerance (diet-induced obese). These epigenetically "preprogrammed" macrophages result in poised macrophages in peripheral tissue and negatively impact wound repair. We found that in diabetic conditions the H3K27 demethylase Jmjd3 drives IL-12 production in macrophages and that IL-12 production can be modulated by inhibiting Jmjd3. Using human T2D tissue and murine models, we have identified a previously unrecognized mechanism by which macrophages are programmed toward a proinflammatory phenotype, establishing a pattern of unrestrained inflammation associated with nonhealing wounds. Hence, histone demethylase inhibitor-based therapy may represent a novel treatment option for 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.