ArticleJCI insight2023
IL-13RA2 downregulation in fibroblasts promotes keloid fibrosis via JAK/STAT6 activation.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 45 citations in OpenAlex.
- Rational design of FAP-targeted sEVs delivered by microneedles for precision treatment of hypertrophic scars via ferroptosis in hypertrophic scar fibroblasts.Materials today. Bio · 2026Article
- Ferroptosis and macrophage polarization: mechanisms, interplay, and implications for medical applications.Cell death discovery · 2026Review
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- IL-13 and skin fibrosis in inflammatory skin diseases.Frontiers in immunology · 2026Review
- The impact of potential food allergen exposure on wound healing after malignant tumor surgery: immune tolerance alterations and clinical risk assessment.Frontiers in immunology · 2026Review
- Mechanistic insights into Strontium-90 superficial radiotherapy in keloids: senescence-associated changes and ECM remodeling across cell-matrix scales.Frontiers in pharmacology · 2026Article
- Potential Causal Association Between Plasma Lipidomes and Keloid: Analysis from a Two-Sample Mendelian Randomization.Clinical, cosmetic and investigational dermatology · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- Eosinophils in lung cancer: from inflammatory cytokines to immunotherapeutic biomarkers.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
- Loss of IL13RA2 promotes metastatic tumor growth in triple-negative breast cancer via increased AKT and NF-κB signaling.Clinical & experimental metastasis · 2025Article
- LA-peptide Hydrogel-Regulation of macrophage and fibroblast fates and their crosstalk via attenuating TGF-β to promote scarless wound healing.Bioactive materials · 2025Article
- Article
- Folate alleviated skin inflammation and fibrosis resulting from impaired homocysteine metabolism.Redox biology · 2025Article
- Moscatilin inhibits vascular calcification by activating IL13RA2-dependent inhibition of STAT3 and attenuating the WNT3/β-catenin signalling pathway.Journal of advanced research · 2025Article
- Effects of exosomes from human dental pulp stem cells on the biological behavior of human fibroblasts.Scientific reports · 2025Article
- Gut microbiota-derived metabolites in keloid and hypertrophic scarring.Frontiers in microbiology · 2025Review
- Orthogonal upconversion supramolecular microneedles promote endogenous ferroptosis in keloids.Theranostics · 2025Article
- Keloids as a Spectrum of Auto-Inflammatory Fibrotic Disorders: Beyond the Conventional Wound-Healing Paradigm.Clinical, cosmetic and investigational dermatology · 2025Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are considered the manifestation of a fibroproliferative disease characterized by chronic inflammation that is induced following skin injury. Deciphering the underlying mechanism of keloid formation is essential for improving treatment outcomes. Here, we found that more macrophages were activated toward the M2 subtype in keloid dermis when compared with normal dermis. Western blotting revealed that the level of phosphorylated STAT6 (p-STAT6), a known inducer of M2 polarization, was higher in keloid fibroblasts as opposed to fibroblasts from normal dermis. Moreover, keloid fibrosis was shown to be positively correlated with the level of p-STAT6. Further, we identified downregulation of IL-13RA2, a decoy receptor for IL-13, in keloid fibroblasts compared with fibroblasts from normal dermis. Ectopic expression of IL-13RA2 in keloid fibroblasts resulted in inhibition of STAT6 phosphorylation, cell proliferation, migration, invasion, extracellular matrix secretion, and myofibroblast marker expression, as well as an increase in apoptosis. Consistently, knockdown of IL-13RA2 in normal fibroblasts induced a keloidal status. Furthermore, both in vitro application and intratumoral injection of p-STAT6 inhibitor AS1517499 in a patient-derived xenograft keloid-implantation mouse model resulted in proliferation inhibition and tissue necrosis, apoptosis, and myofibroblast marker reduction. Collectively, this study elucidates the key role of IL-13RA2 in keloid pathology and inspires further translational research of keloid treatment concerning JAK/STAT6 inhibition.
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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.