Abstract
Acute myocardial infarction (AMI), one of the most severe and fatal cardiovascular diseases, remains the main cause of mortality and morbidity worldwide. The objective of this study is to investigate the potential biomarkers for AMI based on bioinformatics analysis. A total of 2102 differentially expressed genes (DEGs) were screened out from the data obtained from the gene expression omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) explored the co-expression network of DEGs and determined the key module. The brown module was selected as the key one correlated with AMI. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses demonstrated that genes in the brown module were mainly enriched in ‘ribosomal subunit’ and ‘Ribosome’. Gene Set Enrichment Analysis revealed that ‘TNFA_SIGNALING_VIA_NFKB’ was remarkably enriched in AMI. Based on the protein–protein interaction network, ribosomal protein L9 (RPL9) and ribosomal protein L26 (RPL26) were identified as the hub genes. Additionally, the polymerase chain reaction (PCR) results indicated that the expression levels of RPL9 and RPL26 were both downregulated in AMI patients compared with controls, in accordance with the bioinformatics analysis. In summary, the identified DEGs, modules, pathways, and hub genes provide clues and shed light on the potential molecular mechanisms of AMI.
Highlights
According to the updated data of Heart Disease and Stroke Statistics (2020 Edition), cardiovascular disease (CVD) remains the leading cause of death globally, leading to17.8 million deaths worldwide in 2017, which remarkably aggravates the global health burden [1]
As the core component of the immune system, peripheral blood consisting of immune cells, such as lymphocytes, monocytes, and neutrophils, likely regulates the process of Acute myocardial infarction (AMI)
Recent evidence that neutrophil amplifies granulopoiesis after myocardial infarction [4], suggests that identifying the change in peripheral blood during AMI may pave novel therapeutic avenues for AMI
Summary
According to the updated data of Heart Disease and Stroke Statistics (2020 Edition), cardiovascular disease (CVD) remains the leading cause of death globally, leading to17.8 million (95% CI, 17.5–18.0 million) deaths worldwide in 2017, which remarkably aggravates the global health burden [1]. According to the updated data of Heart Disease and Stroke Statistics (2020 Edition), cardiovascular disease (CVD) remains the leading cause of death globally, leading to. Acute myocardial infarction (AMI), one of the most severe cardiovascular diseases, is characterized by the sudden depletion of blood flow to the myocardium, with high morbidity and mortality. As the core component of the immune system, peripheral blood consisting of immune cells, such as lymphocytes, monocytes, and neutrophils, likely regulates the process of AMI. Recent evidence that neutrophil amplifies granulopoiesis after myocardial infarction [4], suggests that identifying the change in peripheral blood during AMI may pave novel therapeutic avenues for AMI
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