Abstract

BackgroundAcute myocardial infarction (AMI), a medical condition caused by the ischemic necrosis of cardiac tissues, is due to sudden occlusion of the coronary arteries in patients including transplant recipients. It is the leading reason for death and disability worldwide. This study aimed to search potential biomarkers related to the progression of AMI and identify the related immune-related pathways, as also examine their association with the immune cell infiltration and diagnostic value for AMI. MethodsDatasets of gene microarray were extracted from (www.ncbi.nlm.nih.gov/geo) the Gene Expression Omnibus (GEO) database and AMI-related biomarkers were obtained by differential expression analysis and weighted correlation network analysis (WGCNA). Subsequently, the support vector machine–recursive feature elimination (SVM–RFE) and the least absolute shrinkage and selection operator (LASSO) regression analyses were used to mine AIM-related hub markers. For the assessment of the diagnostic value of these markers for AMI, the receiver operator characteristic (ROC) curves were plotted. Additionally, the single-sample gene set enrichment analysis (ssGSEA) was performed to determine the immune cell infiltration. ResultsA total of 1273 differentially expressed genes (DEGs) were obtained. Nine co-expression modules were obtained after WGCNA. Among them, the brown-colored module was identified as the hub for AMI (correlation [cor] = 0.73, P = 1.1e-87), and intersected with the DEGs yielded a total of 88 shared genes. Subsequently, five hub genes were obtained from the analysis of the LASSO regression and SVM–RFE algorithm. Ultimately, using the ROC curves, the diagnostic values of these genes for AMI were confirmed. The five hub genes were also found to be significantly associated with the infiltration levels of multiple immune cells. Moreover, the DEGs were mainly enriched in the inflammatory and immune-related gene sets evidenced by the functional enrichment analysis. ConclusionThe five hub genes may serve as potential markers for AMI diagnosis and the findings have implications for further investigations on the molecular mechanisms underlying AMI.

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