Involvement of CCL2 and CH25H Genes and TNF signaling pathways in mast cell activation and pathogenesis of chronic spontaneous urticaria

Chronic spontaneous urticaria (CSU), a mast cell-driven disease, substantially affects the quality of life. While genetics affect CSU susceptibility and severity, specific genetic factors associated with cell activation in remain elusive. We aimed to identify key investigate their roles pathogenesis. Two gene expression datasets from Gene Expression Omnibus were merged validated using principal component analysis boxplots. The dataset was subjected limma weighted co-expression network analyses. Genes whose correlated highly identified analyzed Set Enrichment Analysis (GSEA), Ontology (GO), Kyoto Encyclopedia Genomes (KEGG) enrichment As GSEA, GO, KEGG analyses highlighted importance chemokine (C-C motif) ligand 2 (CCL2) cholesterol 25-hydroxylase (CH25H) tumor necrosis factor (TNF) signaling pathways CSU; three corresponding genes knocked down human line-1 (HMC-1), followed by incubation thrombin mimic CCL2, CH25H, TNF knockdown reduced excitability cytokine production HMC-1. Our findings suggest that involved play crucial pathogenesis, providing insights into potential therapeutic targets for treatment.