Potential Biomarkers of Acute Myocardial Infarction Based on Co-Expression Network Analysis

Abstract Background: Acute myocardial infarction (AMI) is a common cause of death in many countries. Analyzing the potential biomarkers of AMI is crucial to understanding the molecular mechanism of disease. However, specific diagnostic biomarkers have not been fully elucidated, and candidate regulatory targets for AMI have not been determined.Methods: In this study, AMI gene chip data GSE48060, blood samples from normal cardiac function controls (n = 21) and AMI patients (n = 26) were downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) of AMI and control group were identified with Online tool GEO2R. the genes co-expressed with were found. The co-expression network of DEGs was analyzed by calculating the Pearson correlation coefficient of all gene pairs, MR screening and cutoff threshold screening. Then, GO database was used to analyze the function and pathway enrichment of genes in the most important modules. KEGG DISEASE and BioCyc were used to analyze the hub gene in the module to determine important sub-pathways. In addition, the expression of hub genes were certified by RT-qPCR in AMI and control specimens.Results: This study identified 52 DEGs, including 26 up-regulated genes and 26 down-regulated genes. Co-expression network analysis of 52 DEGs revealed that there are mainly three up-regulated genes (AKR1C3, RPS24 and P2RY12) and three down-regulated genes (ACSL1, B3GNT5 and MGAM) as key hub genes in the co-expression network. Furthermore, GO enrichment analysis was performed on all AMI co-expression network genes and found to be functionally enriched mainly in RAGE receptor binding and negative regulation of T cell cytokine production. In addition, through KEGG DISEASE and BioCyc analysis, the functions of genes RPS24 and P2RY12 were enriched in cardiovascular diseases, AKR1C3 was enriched in cardenolide biosynthesis, MGAM was enriched in glycogenolysis, B3GNT5 was enriched in glycosphingolipids biosynthesis, and ACSL1 enriched in icosapentaenoate biosynthesis II. Conclusion: The hub genes AKR1C3, RPS24, P2RY12, ACSL1, B3GNT5 and MGAM are potential targets of AMI and have potential application value in the diagnosis of AMI.