ArticleHeliyon2024
The mechanism of TGF-β mediating BRD4/STAT3 signaling pathway to promote fibroblast proliferation and thus promote keloid progression.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Review
- Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway.International journal of molecular sciences · 2026Review
- Research Advances in Therapeutic Strategies and Drug Delivery Systems for Pathological Scars.Pharmaceutics · 2026Review
- Tubular NAT10 Promotes the Secretion of TGF-β and Lactate to Drive Fibroblast Activation in Diabetic Kidney Disease.International journal of biological sciences · 2026Article
- GLP-1RA in JBMMSCs promoted osteogenic differentiation via modulating CREB and BRD4 signaling mediated proliferation and stemness.Scientific reports · 2025Article
- Comparative analysis of Microtus fortis and murine hosts reveals a correlation between BRD4 and hepatic inflammation during Schistosoma japonicum infection.Parasites & vectors · 2025Article
- Machine learning-based integration of DCE-MRI radiomics for STAT3 expression prediction and survival stratification in breast cancer.Frontiers in immunology · 2025Article
- Glutamate enhances the production of inflammatory cytokines IL-6 and IL-11, as well as chemokines CXCL2, CXCL3, and CXCL8 in keloid fibroblasts.Frontiers in molecular biosciences · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study was to investigate the effect of TGF-β on keloid and its molecular mechanism in fibroblasts.
methodsThe difference between normal tissue and keloid tissue can be detected using HE staining. Fibroblasts were treated with TGF-β, and then treated with the BRD4 inhibitor JQ1 and the STAT3 activator Colivelin TFA. Western blot was used to measure the relative protein expression of TGF-β, BRD4, p-STAT3, p-EZH2, C-myc, KLF2, KLF4, α-SMA, and Collagen-I. Immunofluorescence staining was used to measure the relative fluorescence intensity of BRD4, p-STAT3, α-SMA, and Collagen-I. Cell proliferation ability was evaluated by CCK-8 assay and colony formation assay.
resultsThe expression of TGF-β and BRD4 was significantly higher in keloid tissue compared to normal tissue. TGF-β mediated the BRD4/STAT3 signaling pathway to inhibit p-EZH2 and promote the expression of C-myc, KLF2, KLF4, α-SMA, and Collagen-I. Additionally, TGF-β mediated the BRD4/STAT3 signaling pathway to enhance fibroblast proliferation.
conclusionTGF-β mediates the BRD4/STAT3 signaling pathway to promote fibroblast proliferation and contribute to the progression of keloid.
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