Evidence shows that primary gout is prone to develop to atherosclerosis, but the mechanism of its occurrence is still not fully clarified. The aim of this study was to explore the molecular mechanism of the occurrence of this complication in gout. The gene expression profiles of primary gout and atherosclerosis were downloaded from the gene expression omnibus database. Overlapping differentially expressed genes (DEGs) between gout and atherosclerosis were identified. The biological roles of common DEGs were explored through enrichment analyses. Hub genes were identified using protein-protein interaction networks. The immune infiltrations of 28 types of immune cells in gout and control samples from GSE160170 were evaluated by the ssGSEA method. Transcription factors (TFs) were predicted using Transcriptional Regulatory Relationships Unraveled by Sentence Based Text Mining (TRRUST) database. A total of 168 overlapping DEGs were identified. Functional enrichment analyses indicated that DEGs were mostly enriched in chemokine signaling pathway, regulation of actin cytoskeleton, and TNF signaling pathway. CytoScape demonstrated 11 hub genes and two gene cluster modules. The immune infiltration analysis showed that the expression of DEGs in gout was significantly upregulated in activated CD4 T cells, gamma delta T cells, T follicular helper cell, CD56dim natural killer cells, and eosinophil. TRRUST predicted one TF, RUNX family transcription factor 1. Our study explored the pathogenesis of gout with atherosclerosis and discovered the immune infiltration of gout. These results may guide future experimental research and clinical transformation.
© 2024. The Author(s).