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Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway
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Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway
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Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway
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Journal Article
Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway
2025
Overview
Background and Objectives
Keloids are problematic fibrotic lesions with excessive collagen and chronic inflammation; their underlying causes are not fully understood. Type 2 helper T (Th2) cytokines IL-4 and IL-13 are implicated in various fibrotic disorders, including but not limited to pulmonary fibrosis and systemic sclerosis. This study aimed to investigate the IL-4/IL-13 signaling pathway's contribution to keloid pathophysiology and evaluate its potential as a novel therapeutic target.
Methods
We retrospectively analyzed keloid patients, collecting demographic data and grading scar severity with the Vancouver Scar Scale (VSS). Keloid tissue specimens underwent immunofluorescence, Western blotting, and real-time PCR to quantify IL-4, IL-13, Type I Collagen alpha 1 (Collagen I A1), and phosphorylated STAT6 (p-STAT6) expression.
Results
Patients had an average total VSS score of 11.0 ± 2.9, indicating active fibrotic inflammation. Molecular assays showed significant upregulation of IL-4 and IL-13, alongside increased p-STAT6 and Collagen I A1 in keloid tissues. Notably, IL-4, IL-13, and p-STAT6 expression positively correlated with VSS thickness and pliability scores.
Conclusions
Our findings demonstrate that the IL-4/IL-13 signaling axis is markedly activated in keloid tissues, promoting collagen synthesis via STAT6 phosphorylation. Therefore, targeting the IL-4/IL-13/STAT6 pathway may represent a promising therapeutic strategy for managing keloids.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
