Exploring the Pathogenesis of Psoriasis Complicated With Atherosclerosis via Microarray Data Analysis

Background Although more and more evidence has supported psoriasis is prone to atherosclerosis, the common mechanism of its occurrence is still not fully elucidated. The purpose of this study is to further explore the molecular mechanism of the occurrence of this complication. Methods The gene expression profiles of psoriasis (GSE30999) and atherosclerosis (GSE28829) were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the common differentially expressed genes (DEGs) of psoriasis and atherosclerosis, three kinds of analyses were performed, namely functional annotation, protein-protein interaction (PPI) network and module construction, and hub gene identification and co-expression analysis. Results A total of 94 common DEGs (24 downregulated genes and 70 upregulated genes) was selected for subsequent analyses. Functional analysis emphasizes the important role of chemokines and cytokines in these two diseases. In addition, lipopolysaccharide-mediated signaling pathway is closely related to both. Finally, 16 important hub genes were identified using cytoHubba, including LYN, CSF2RB, IL1RN, RAC2, CCL5, IRF8, C1QB, MMP9, PLEK, PTPRC, FYB, BCL2A1, LCP2, CD53, NCF2 and TLR2. Conclusions Our study reveals the common pathogenesis of psoriasis and atherosclerosis. These common pathways and hub genes may provide new ideas for further mechanism research.

Automated summary

This study identified common differentially expressed genes in psoriasis and atherosclerosis, highlighting the important roles of chemokines and cytokines in both diseases. The study also found that the lipopolysaccharide-mediated signaling pathway is closely related to both diseases. Furthermore, 16 important hub genes were identified which may provide new insights for further mechanism research.