identification of potential molecular mechanisms and candidate genes involved in the acute p hase of myocardial infarction

Objective: this study used bioinformatics to determine genetic factors involved in progression of acute myocardial infarction (mi). materials and methods: in this prospective study, gene expression profile gse59867 was downloaded from the gene expression omnibus database, which contained 46 normal samples obtained from stable coronary artery disease patients (n=46) who were without history of mi (control) and 390 samples from patients (n=111) who had evolving st-segment elevation myocardial infarction (stemi) as the mi group. these samples were divided into 4 groups based on time points. after identification of differentially expressed genes (degs), we conducted hierarchical clustering and functional enrichment analysis. protein interaction and transcriptional regulation among degs were analysed. results: we observed 8 clusters of degs that had a peak or a minimum at the t=1 time point according to gene expression levels. upregulated degs showed significant enrichment in the biological process, single-organism cellular process, response to stimulus and stress, and osteoclast differentiation and lysosome. downregulated degs enriched in the t-cell receptor signalling pathway and natural killer cell mediated cytotoxicity. we identified multiple genes, including signal transducer and activator of transcription 3 (stat3); lck proto-oncogene, src family tyrosine kinase (lck); and fyn proto-oncogene, src family tyrosine kinase (fyn) from the protein-protein interaction (ppi) network and/or the transcriptional regulatory network. conclusion: cytokine-mediated inflammation, lysosome and osteoclast differentiation, and metabolism processes, as well as stat3 may be involved in the acute phase of mi.