Unveiling shared therapeutic targets and pathological pathways between coronary artery disease and major depressive disorder through bioinformatics analysis.

Coronary artery disease (CAD) is a predominant cardiovascular condition influenced by risk factors, with an emphasis on major depressive disorder (MDD). However, the shared mechanisms and therapeutic targets for CAD and MDD remain incompletely comprehended. Functional enrichment analyses were conducted to investigate the pathways associated with the differentially expressed genes (DEGs) in the CAD and MDD datasets. Hub genes were identified utilizing the Protein-Protein Interaction network and Cytoscape software. The single sample gene set variation analysis was applied to assess immune cell infiltration in the CAD and MDD datasets. Weighted gene co-expression network analysis and molecular biological experiments were executed to evaluate these hub genes. Molecular docking was conducted to identify drug candidates targeting these hub genes. The overlapping DEGs between the CAD and MDD datasets were mainly enriched in the Herpes simplex virus 1 infection and the NF-kappa B signaling pathways. CDC42, NDUFB3, and TXN were validated within the eigengenes of the blue module, which exhibited a significant association with the CAD phenotype. The drug candidate GS-9620 was identified as a potential protective agent against both disorders. In conclusion, CDC42, NDUFB3, and TXN held potential as molecular biomarkers and therapeutic targets for the simultaneous treatment of CAD and MDD.