Identification of potential biomarkers and therapeutic targets in the chronic obstructive pulmonary disease and acute myocardial infarction

Abstract

Background Chronic obstructive pulmonary disease (COPD) and acute myocardial infarction (AMI) have a strong association. We aimed to study the relationships between COPD and AMI, and reveal potential therapeutic targets and biomarkers. , Methods The dataset GSE38974 and GSE60993 were downloaded from the Gene Expression Omnibus (GEO) database to analyze the intersections among differentially expressed genes (DEGs). Common DEGs were identified and performed functional enrichment analyses. The hub genes were obtained based on the protein-protein interaction (PPI) network by cytoHubba in Cytoscape software. The receiver operator characteristic (ROC) curve analysis was applied to identify the diagnosis efficacy of hub genes. The relationship between hub genes and these two diseases in the CTD database were validated. Finally, the transcription factors (TFs) corresponding to hub genes were also analyzed. Results In our study, sixty-five common DEGs were obtained in COPD and AMI. GO enrichment analysis indicated that inflammation or apoptotic biological processes are significant enriched biological processes. Common DEGs were mostly enriched in pathways including apoptosis, HIF-1 signaling pathway, TNF signaling pathway, and cytokine-cytokine receptor interaction. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes. Furthermore, we found that the expression of hub genes was significantly associated with a diagnosis efficacy of COPD and AMI. We also validated the relationship between the hub genes and these two diseases in the CTD database. We also found that ELK1, ETV4, STAT3 and TFAP2A were significant TFs, which interacted with the hub genes. Conclusions In conclusion, our study revealed the communal DEGs and related mechanisms between the pathophysiology of COPD and AMI. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes that are associated with COPD and AMI. Our study provides new ideas and evidence for further exploration of the mechanisms and treatment of COPD and AMI.