Abstract
BACKGROUND: Gout is a type of chronic inflammatory disease linked to the accumulation of monosodium urate crystals, leading to arthritis. Studies have shown that patients with gout are more likely to develop atherosclerosis, but the specific mechanisms involved remain unknown. The purpose of the research was to explore the key molecules and potential mechanisms between gout and atherosclerosis. METHODS: Gene expression profiles for gout as well as atherosclerosis were obtained from the Gene Expression Omnibus (GEO) database, then differential analysis was utilized to identify common differentially expressed genes (DEGs) between the two diseases. The analysis of functional enrichment was conducted to investigate the biological processes that the DEGs might be involved in. The Cytoscape software was utilized to develop a protein-protein interaction (PPI) network as well as identify hub genes, while LASSO analysis was employed to select key genes. The TRRUST database was utilized to forecast transcription factors (TFs), and the miRTarBase database was utilized to forecast miRNAs. RESULTS: Four key genes, CCL3, TNF, CCR2, and CCR5, were identified. The receiver operating characteristic (ROC) curves showed that the areas under ROC curve (AUC) for these four key genes in both gout and atherosclerosis were greater than 0.9. The analysis of functional enrichment revealed that the DEGs were primarily involved in "regulation of T-cell activation", "chemokine signaling pathway", and other biological processes. The TRRUST prediction results indicated that RELA and NFKB1 are common regulatory transcription factors for CCR2, CCR5, CCL3, and TNF. The miRTarBase prediction results showed that hsa-miR-203a-3p is a common regulatory miRNA for TNF and CCR5. CONCLUSION: This study preliminarily explored the potential key molecules and mechanisms between gout and atherosclerosis. These findings provide new insights for further research into identifying potential biomarkers and clinical treatment strategies for these two diseases.