Machine learning-based bioinformatics analysis of common hub genes associated with oxidative stress and immune infiltration in COPD and atherosclerosis 

Abstract Background Chronic obstructive pulmonary disease (COPD) and atherosclerosis (AS) are both chronic irreversible diseases in the aged population, with oxidative stress (OS) and immune activation as the pathological basis. This study explored the common hub gene associated with OS and immune cell infiltration in AS and COPD. Methods Genes associated with AS were identified by the differentially expressed genes (DEGs) analysis and weighted gene co‑expression network analysis (WGCNA) in the GSE100927 dataset. Genes associated with COPD were analyzed by WGCNA in the GSE76925 dataset. Functional enrichment analysis was carried out by Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). The common hub OS-related genes were analyzed by the intersection of the WGCNA modules of AS and COPD and OS‑related genes, protein–protein interaction (PPI), and lasso regression. The diagnostic value of the hub common genes was assessed by receiver operating characteristic analysis. The association of the hub common genes with immune infiltration in AS and COPD was analyzed by the Spearman correlation method. Results A total of 455 DEGs (336 upregulated genes and 139 downregulated genes) were identified in GSE100927. The turquoise module of WGCNA in GSE100927 and the yellow module of WGCNA in GSE76925, which are the most relevant modules, were intersected and obtained 25 common OS-related genes between AS and COPD. Those common OS-related genes were enriched in signaling pathways related to immunity and OS. Two hub common OS-related genes (SELL and MMP9) were identified and showed good diagnostic value in AS and COPD. The Spearman correlation analysis showed that the hub common OS-related genes positively or negatively correlated with various infiltrating immune cells. Conclusion Our study identified the common hub genes (SELL and MMP9) associated with OS and immune infiltration in AS and COPD, providing candidate therapeutic targets for AS combined with COPD.