Deciphering the Molecular Mechanisms Underlying the Psoriasis and T2D: A Systems Biology Approach Using Microarray Data Analysis
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Abstract
Background: Although a large number of evidence has identified that psoriasis is significantly correlated with type 2 diabetes (T2D), the common molecular mechanism of its occurrence remains unclear. Our study aims to further elucidate the mechanism of the occurrence of this complication. Methods: We obtained the gene expression data of psoriasis (GSE30999) and T2D (GSE28829) from the Gene Expression Omnibus (GEO) dataset. Then the common differentially expressed genes (DEGs) of T2D and psoriasis were identified. After that, we performed three types of analyses about these DEGs, including functional enrichment analysis, protein-protein interaction (PPI) network and module manufacture, hub genes identification and co-expression analysis. Results: 132 common DEGs (14 upregulated genes and 118 downregulated genes) were identified for subsequent a series of analyses. Function enrichment analysis demonstrated that Rap1 signaling pathway, PI3K-Akt signaling pathway, and cGMP-PKG signaling pathway may play a significant role in pathogenesis of psoriasis and T2D. Finally, 3 important hub genes were selected by utilizing cytoHubba, including SNRPN, GNAS, IGF2. Conclusions: Our work reveals the common pathogenesis of psoriasis and T2D. These Hub genes and common signaling pathways provide insights for further investigation of molecular mechanism about psoriasis and T2D.
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