ArticleBurns & trauma2022
WNT5A drives interleukin-6-dependent epithelial-mesenchymal transition via the JAK/STAT pathway in keloid pathogenesis.
Article in Burns & trauma, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Systematic review of dupilumab safety and efficacy for treatment of keloid scars.Archives of dermatological research · 2024Pooled it
- Beryllium Sulfate-Induced Cellular Senescence via the IL-6/STAT3 Pathway to Promote Pulmonary Fibrosis.Journal of applied toxicology : JAT · 2026Article
- Comprehensive Transcriptomic Profiling of Nonatopic Prurigo Nodularis in Korean Patients Reveals Il-22-driven Epidermal Stress and Neuro-immuno-fibrotic Remodelling.Acta dermato-venereologica · 2026Article
- Integrative multiomics analysis identifies RARRES2 as a regulator of keloid pathogenesis through STAT3/HSPG2 signaling axis.iScience · 2026Article
- Metabolic reprogramming and ferroptosis in keloid pathogenesis: new insights for targeted therapy.Molecular biology reports · 2026Review
- 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
- Spatiotemporal dynamics of mammalian wound healing.Cell discovery · 2026Review
- Single-Cell RNA-Seq Reveals a Glycolysis-Biased EMT State in Keloid Keratinocytes That Amplifies the Pro-Inflammatory and Fibrotic Microenvironment.Journal of inflammation research · 2026Article
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- Mesenchymal Stem Cells-Derived Exosomes: Next-Generation Nanomedicines Toward Scarless Wound Healing.International journal of nanomedicine · 2026Review
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
- A novel CAVIN1/GAS5 axis suppresses skin fibrosis through mitochondrial fission-mediated attenuation of the TGF-β/Smad pathway.Burns & trauma · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- A panoramic analysis of keloid pathogenesis: multidimensional network regulation of genetics-immunity-metabolism-mechanical force.Frontiers in immunology · 2026Review
- Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway.European journal of medical research · 2025Article
- SPP1Scientific reports · 2025Article
- Targeting WNT5A noncanonical signaling attenuates renal fibrosis progression in acute kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Uncovering a fibroblast differentiation-based keloid classification by integration of single-cell and bulk RNA sequencing.Communications biology · 2025Article
- Integrative analysis identifies FERMT3 as a key regulator of metabolic reprogramming in keloid scarring and metabolic syndrome.Functional & integrative genomics · 2025Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Keloid scarring is a fibroproliferative disease caused by aberrant genetic activation with an unclear underlying mechanism. Genetic predisposition, aberrant cellular responses to environmental factors, increased inflammatory cytokines and epithelial-mesenchymal transition (EMT) phenomena are known as major contributors. In this study, we aimed to identify the molecular drivers that initiate keloid pathogenesis. Methods: Bulk tissue RNA sequencing analyses of keloid and normal tissues along with Results: Gene set enrichment analysis revealed upregulation of Wnt family member 5A ( Conclusions: Intercellular communication via the WNT5A and STAT pathways possibly underlies a partial mechanism of EMT-like phenomena in keloid pathogenesis. IL-6 secreted from WNT5A-activated fibroblasts or keloid fibroblasts activates the JAK/STAT signaling pathway in adjacent keratinocytes which in turn express EMT markers. A better understanding of keloid development and the role of WNT5A in EMT will promote the development of next-generation targeted treatments for keloid scars.
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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.