ArticleExperimental dermatology2019
STAT3 signalling pathway is implicated in keloid pathogenesis by preliminary transcriptome and open chromatin analyses.
Article in Experimental dermatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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
28 citing papers in PubMed, 47 citations in OpenAlex.
- Differential responses to folic acid in an established keloid fibroblast cell line are mediated by JAK1/2 and STAT3.PloS one · 2021Trial
- 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
- Post-translational modifications of collagen and its related diseases in metabolic pathways.Acta pharmaceutica Sinica. B · 2025Review
- Periostin regulates the activity of keloid fibroblasts by activating the JAK/STAT signaling pathway.Heliyon · 2024Article
- Update on the Pathogenesis of Keloid Formation.JID innovations : skin science from molecules to population health · 2024Review
- Comprehensive Insights into Keloid Pathogenesis and Advanced Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Roles and Mechanisms of miRNAs in Abdominal Aortic Aneurysm: Signaling Pathways and Clinical Insights.Current atherosclerosis reports · 2024Review
- Profibrotic Inflammatory Cytokines and Growth Factors Are Predicted as the Key Targets ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Exosomes: A Promising Strategy for Repair, Regeneration and Treatment of Skin Disorders.Cells · 2023Review
- FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c-Myc expression.International wound journal · 2023Article
- An updated review of the immunological mechanisms of keloid scars.Frontiers in immunology · 2023Review
- ASC-J9 Blocks Cell Proliferation and Extracellular Matrix Production of Keloid Fibroblasts through Inhibiting STAT3 Signaling.International journal of molecular sciences · 2022Article
- WNT5A drives interleukin-6-dependent epithelial-mesenchymal transition via the JAK/STAT pathway in keloid pathogenesis.Burns & trauma · 2022Article
- Tauroursodeoxycholic Acid Decreases Keloid Formation by Reducing Endoplasmic Reticulum Stress as Implicated in the Pathogenesis of Keloid.International journal of molecular sciences · 2021Article
- Skin epigenetics.Experimental dermatology · 2021Article
- [Roles of interleukin-6/signal transduction and activator of transcription 3 pathway andZhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Article
- Fostering a healthy culture: Biological relevance of in vitro and ex vivo skin models.Experimental dermatology · 2021Article
- Inference and analysis of cell-cell communication using CellChat.Nature communications · 2021Article
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Keloids are wounding-induced fibroproliferative human tumor-like skin scars of complex genetic makeup and poorly defined pathogenesis. To reveal dynamic epigenetic and transcriptome changes of keloid fibroblasts, we performed RNA-seq and ATAC-seq analysis on an early passage keloid fibroblast cell strain and its paired normal control fibroblasts. This keloid strain produced keloid-like scars in a plasma clot-based skin equivalent humanized keloid animal model. RNA-seq analysis reveals gene ontology terms including hepatic fibrosis, Wnt-β-catenin, TGF-β, regulation of epithelial-mesenchymal transition (EMT), STAT3 and adherens junction. ATAC-seq analysis suggests STAT3 signalling is the most significantly enriched gene ontology term in keloid fibroblasts, followed by Wnt signalling (Wnt5) and regulation of the EMT pathway. Immunohistochemistry confirms that STAT3 (Tyr705 phospho-STAT3) is activated and β-catenin is up-regulated in the dermis of keloid clinical specimens and keloid skin equivalent implants from the humanized mouse model. A non-linear dose-response of cucurbitacin I, a selective JAK2/STAT3 inhibitor, in collagen type I expression of keloid-derived plasma clot-based skin equivalents implicates a likely role of STAT3 signalling in keloid pathogenesis. This work also demonstrates the utility of the recently established humanized keloid mouse model in exploring the mechanism of keloid formation.
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Registered trials
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