Bioinformatics screening of potential pathways and targets related to myocardial ischemia-reperfusion injury in rats based on GEO database
Objective:To screen key genes (Hub genes), pathways, and drug candidates related to myocardial ischemia-reperfusion injury (MIRI) in rats by bioinformatics analysis based on the gene expression omnibus (GEO) database.Methods:The rat GSE122020 dataset was downloaded from the GEO database and differentially expressed genes (DEGs) were screened using the GEO2R online tool. Pathophysiological processes and potential signaling pathways involved in MIRI-related DEGs were investigated by Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The MIRI-related DEGs protein-protein interaction (PPI) network was constructed using databases such as STRING, and the key genes in the PPI network were screened and visualized using Cytoscape software. Potential drug candidates for key genes were screened using the Enrichr database.Results:A total of 377 differential genes were screened, of which 109 were up-regulated and 268 down-regulated. KEGG pathway enrichment analysis showed that the up-regulated 109 genes were enriched in six pathways including the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway, while the 268 down-regulated genes were enriched in 58 pathways including the tumor necrosis factor (TNF) signaling pathway. Combined analysis based on the STRING and Gene MANIA databases and Cytoscape software resulted in the identification of 20 key DEGs, of which 4 were up-regulated and 16 down-reglated. For the 4 up-regulated genes, 55 potential drugs including nicotinic acid and quercetin were predicted based on the DSigDB database in the Enrichr database, while for the 16 down-regulated genes, 92 potential drugs including 3,3'-diindolylmethane and potassium dichromate were predicted.Conclusion:Through bioinformatics methods, the pathogenic genes of MIRI can be effectively discovered, which provides new ideas and entry points for further exploring the molecular mechanism and therapeutic targets for MIRI.
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