Evidence map›Paper›PMID 41408341›Full record

ArticleEuropean journal of medical research2025

Exploration of novel therapeutic targets for keloids based on clinical and molecular data: the role of the IL-4/IL-13 signaling pathway.

Xueli Li, Jianping Lan, Ruoyun Liu, Tingting Lin, Zheqi Li, Bo Cheng

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Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors.

Xueli LiDepartment of Dermatology, The First Affiliated Hospital of Fujian Medical University, 20 Chazhong Road, Fuzhou, 350000, Fujian, China.
Jianping LanDepartment of Dermatology, Mindong Hospital affiliated to Fujian Medical University, Ningde, 355000, Fujian, China.
Ruoyun LiuDepartment of Dermatology, Mindong Hospital affiliated to Fujian Medical University, Ningde, 355000, Fujian, China.
Tingting LinDepartment of Dermatology, Mindong Hospital affiliated to Fujian Medical University, Ningde, 355000, Fujian, China.
Zheqi LiDepartment of Dermatology, Mindong Hospital affiliated to Fujian Medical University, Ningde, 355000, Fujian, China.
Bo ChengDepartment of Dermatology, The First Affiliated Hospital of Fujian Medical University, 20 Chazhong Road, Fuzhou, 350000, Fujian, China. chengbo630415@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesKeloids 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.

methodsWe 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.

resultsPatients 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.

conclusionsOur 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.

Indexed as

Interleukin-13Interleukin-4KeloidSignal TransductionAdultCollagen Type IFemaleHumansMaleMiddle AgedRetrospective StudiesSTAT6 Transcription FactorYoung AdultCollagen Type IIL13 protein, humanIL4 protein, humanInterleukin-13Interleukin-4STAT6 protein, humanSTAT6 Transcription FactorFibrosisInterleukin-13Interleukin-4KeloidSTAT6Therapeutic targets

Identifiers

PMID41408341
PMCPMC12814583

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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.