ArticleDiabetes2019
Diabetes-Induced NF-κB Dysregulation in Skeletal Stem Cells Prevents Resolution of Inflammation.
Article in Diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- Skeletal stem and progenitor cell niche organization, regulation and repair.Reviews in endocrine & metabolic disorders · 2026Review
- Role of the immune microenvironment in bone regeneration and progress in immune-modulating bone nanobiomaterials.Journal of Zhejiang University. Science. B · 2026Review
- Nutritional Interventions to Optimize Orthobiologic Therapy Quality in Type 2 Diabetes Mellitus: Molecular Mechanisms and Clinical Framework: A Narrative Review.International journal of molecular sciences · 2026Review
- Article
- Association of preoperative fasting blood glucose with 1-year Harris Hip Score after hip fracture in older adults: a multicenter retrospective cohort study.Frontiers in endocrinology · 2026Observational
- Application of Biomaterials in Diabetic Wound Healing: The Recent Advances and Pathological Aspects.Pharmaceutics · 2025Review
- Glabridin Alleviates Oxidative Stress-Induced Osteoporosis by Targeting the Akt/NF-ĸB and Akt/GSK-3β Pathways.International journal of molecular sciences · 2025Article
- Primed inflammatory response by fibroblast subset is necessary for proper oral and cutaneous wound healing.Molecular oral microbiology · 2024Article
- IL-17RA Signaling in Prx1+ Mesenchymal Cells Influences Fracture Healing in Mice.International journal of molecular sciences · 2024Article
- Advantages and Limitations of Diabetic Bone Healing in Mouse Models: A Narrative Review.Biomedicines · 2023Review
- DNA methylation-mediated Rbpjk suppression protects against fracture nonunion caused by systemic inflammation.The Journal of clinical investigation · 2023Article
- Dual stimulus responsive borosilicate glass (BSG) scaffolds promote diabetic alveolar bone defectsrepair by modulating macrophage phenotype.Bioactive materials · 2023Article
- Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway.Diabetology & metabolic syndrome · 2023Article
- Osteoimmunology in Periodontitis and Orthodontic Tooth Movement.Current osteoporosis reports · 2023Review
- Distinct fibroblast progenitor subpopulation expedites regenerative mucosal healing by immunomodulation.The Journal of experimental medicine · 2023Article
- Accelerated Wound Healing in Diabetic Rat by miRNA-185-5p and Its Anti-Inflammatory Activity.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- FOXO 1 deletion in chondrocytes rescues diabetes-impaired fracture healing by restoring angiogenesis and reducing apoptosis.Frontiers in endocrinology · 2023Article
- Diabetes and Impaired Fracture Healing: A Narrative Review of Recent Literature.Current osteoporosis reports · 2022Review
- Loss of Bcl-3 delays bone fracture healing through activating NF-κB signaling in mesenchymal stem cells.Journal of orthopaedic translation · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Type 1 diabetes (T1D) imposes a significant health burden by negatively affecting tissue regeneration during wound healing. The adverse effect of diabetes is attributed to high levels of inflammation, but the cellular mechanisms responsible remain elusive. In this study, we show that intrinsic skeletal stem cells (SSCs), a subset of mesenchymal stem cells, are essential for resolution of inflammation to occur during osseous healing by using genetic approaches to selectively ablate SSCs. T1D caused aberrant nuclear factor-κB (NF-κB) activation in SSCs and substantially enhanced inflammation in vivo. Constitutive or tamoxifen-induced inhibition of NF-κB in SSCs rescued the impact of diabetes on inflammation, SSC expansion, and tissue formation. In contrast, NF-κB inhibition in chondrocytes failed to reverse the effect of T1D. Mechanistically, diabetes caused defective proresolving macrophage (M2) polarization by reducing TGF-β1 expression by SSCs, which was recovered by NF-κB inhibition or exogenous TGF-β1 treatment. These data identify an underlying mechanism for altered healing in T1D and demonstrate that diabetes induces NF-κB hyperactivation in SSCs to disrupt their ability to modulate M2 polarization and resolve inflammation.
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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.