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Integrated Transcriptomic and Proteomic Profiling in keloid tissue from patients with keloids

biochemistry
bioinformatics
cell-biology
dermatology
pathology

Abstract

Background: Keloid is a pathological skin fibrosis disease characterized by abnormal proliferation of dermal fibroblasts and excessive deposition of extracellular matrix (ECM). Its high recurrence rate necessitates an in-depth investigation of molecular mechanisms to develop effective treatment strategies.

Methods: In this study, 20 samples of keloid tissue and adjacent normal skin were collected. Transcriptome sequencing and proteome analysis were performed, combined with differential expression analysis, functional enrichment, weighted gene co-expression network analysis (WGCNA), and protein interaction network analysis using STRING, to systematically explore the molecular characteristics of keloid.

Results: A total of 4994 genes and 828 proteins were found to be differentially expressed in keloid tissue, with enrichment primarily observed in the PI3K-AKT, TGF-β, ECM-receptor interaction, and MAPK signaling pathways. Upregulated hub genes such as MAGED1, FN1, and COL5A2, as well as downregulated hub genes including IL20RA and CLDN4, were identified by WGCNA. Their respective interaction networks were associated with excessive ECM accumulation and disruption of epidermal structure.

Conclusion: This study reveals the regulatory network of epidermal dysfunction caused by excessive activation of fibroblasts in keloids through multi-omics integration, which provides a theoretical basis for multi-target therapy targeting ECM remodeling and PI3K-AKT/MAPK pathway.

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