ArticleJournal of cardiovascular development and disease2022
The Identification and Validation of Hub Genes Associated with Acute Myocardial Infarction Using Weighted Gene Co-Expression Network Analysis.
Article in Journal of cardiovascular development and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
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- Bioinformatics and Experimental Validation of Diagnostic Marker Genes for Myocardial Infarction and Analysis of Their Immune Cell Infiltration.Biochemical genetics · 2026Article
- Identification of biomarkers associated with mitochondria and macrophage polarization in acute myocardial infarction: a bioinformatics analysis and validation study.Journal of cardiothoracic surgery · 2026Article
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- Integrated expression quantitative trait loci and Mendelian randomization analyses of the candidate genes and pathways identified for myocardial infarction.Frontiers in molecular biosciences · 2026Article
- Proteomic and morphologic characterization of ovine macrophage differentiation and polarization.Scientific reports · 2025Article
- PLAC8 as a potential therapeutic target for myocardial infarction: unraveling the molecular mechanisms.Journal of physiology and biochemistry · 2025Article
- PU.1 regulation of type 1 dendritic cell function via NF-κB pathway in inhibition of non-small cell lung cancer progression.Journal of pharmaceutical analysis · 2025Article
- Bioinformatics-based prediction of hsa-miR-4651 and hsa-miR-608 as novel biomarkers for diagnosing silicosis.Biomarkers in medicine · 2025Article
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- Identification of key genes associated with muscle atrophy after spinal cord injury and experimental verification in rats.Frontiers in immunology · 2025Article
- Comparative proteomic profiling of the ovine and human PBMC inflammatory response.Scientific reports · 2024Article
- The identification of hub genes associated with pure ground glass nodules using weighted gene co-expression network analysis.BMC pulmonary medicine · 2024Article
- Ribosome biogenesis in disease: new players and therapeutic targets.Signal transduction and targeted therapy · 2023Review
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- A plasma proteomic approach in patients with heart failure after acute myocardial infarction: insights into the pathogenesis and progression of the disease.Frontiers in cardiovascular medicine · 2023Article
- Identification and validation of senescence-related genes in circulating endothelial cells of patients with acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
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.
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