ArticleInflammation2020
IL-17 Induced Stromal Cell-Derived Factor-1 and Profibrotic Factor in Keloid-Derived Skin Fibroblasts via the STAT3 Pathway.
Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
The trial behind it
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
36 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The role of IL-17 and Th17 cells in keloid pathogenesis.Archives of dermatological research · 2024Pooled it
- The role of IL-17 and Th17 cells in keloid pathogenesis.Archives of dermatological research · 2024Pooled it
- Research advances in the pathogenesis and photodynamic therapy of pathological scars.Lasers in medical science · 2026Review
- LncRNA RNF144A-AS1 increases P300-mediated H4K5 acetylation of PDE4 to promote keloid fibrosis.Biomedical engineering online · 2026Article
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- Immune-dominated cellular heterogeneity and stromal plasticity in keloid infiltrating and hypercellular zones revealed by single-cell RNA sequencing.Frontiers in immunology · 2026Article
- Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Regulatory role of POSTN in keloid pathogenesis.Molecular medicine reports · 2025Article
- Cascade-targeting pH/ROS microneedles promote scarless diabetic wound healing by macrophage metaboimmune reprogramming.Science advances · 2025Article
- Keloids as a Spectrum of Auto-Inflammatory Fibrotic Disorders: Beyond the Conventional Wound-Healing Paradigm.Clinical, cosmetic and investigational dermatology · 2025Review
- Adipose stem cell exosomes promote mitochondrial autophagy through the PI3K/AKT/mTOR pathway to alleviate keloids.Stem cell research & therapy · 2024Article
- Monoclonal Antibodies in the Management of Inflammation in Wound Healing: An Updated Literature Review.Journal of clinical medicine · 2024Review
- Identification of inflammation-related biomarkers in keloids.Frontiers in immunology · 2024Article
- Single-cell RNA-seq reveals immune cell heterogeneity and increased Th17 cells in human fibrotic skin diseases.Frontiers in immunology · 2024Article
- Identification of a potential bioinformatics-based biomarker in keloids and its correlation with immune infiltration.European journal of medical research · 2023Article
- Autocrine IL-6 drives cell and extracellular matrix anisotropy in scar fibroblasts.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Tissue RNA Sequencing Reveals Novel Biomarkers Associated with Postoperative Keloid Recurrence.Journal of clinical medicine · 2023Article
- Review
- Establishment of a humanized mouse model of keloid diseases following the migration of patient immune cells to the lesion: Patient-derived keloid xenograft (PDKX) model.Experimental & molecular medicine · 2023Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The pathogenesis of keloids has not been elucidated, and the disease is thought to be caused by abnormal secretion of proinflammatory mediators and irregular responses to other inflammatory signals mediated by keloid fibroblasts (KFs). In this study, we investigated whether a local increase in interleukin IL-17 in keloid tissues stimulates the production of stromal cell-derived factor-1 (SDF-1) in KFs causing further recruitment of IL-17-producing T helper 17 (Th17) cells, which subsequently creates a positive feedback loop. Histological assessment was performed and the change in the expression of IL-17, IL-1β, IL-6, and TNF-α which of fibrosis and inflammation associated markers was examined. In addition, fibroblasts were treated with IL-17 in the presence or absence of STAT3 inhibitor STA-21; SDF-1 levels and fibrosis genes were measured. Our results showed that fibrotic reaction and expression of proinflammatory cytokines including IL-17 were most prominent in the growing margin (perilesional area) of keloid tissue and Th17 cells significantly infiltrated the perilesional area. In addition, IL-17 upregulated the expression of SDF-1, collagen, and α-SMA in KFs. Finally, STA-21 decreased SDF-1α expression and the expression of fibrosis genes in KFs even after IL-17 stimulation. Our study demonstrated that a local increase in IL-17 in keloid tissues stimulates the production of SDF-1 in KFs causing further recruitment of IL-17-producing T helper 17 (Th17) cells, which subsequently creates a positive feedback loop. These findings suggest that STAT3 inhibition can be used to treat keloid scars by reversing the vicious cycle between Th17 cells and KFs.
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