Bioinformatics analysis of key genes and signaling pathways associated with myocardial infarction following telomerase activation.

The present study aimed to identify key genes and signaling pathways associated with myocardial infarction (MI) following telomerase activation, and investigate the possible underlying molecular mechanisms involved in this process. Array data of GSE62973 was downloaded, including 11 samples from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were analyzed in infarct vs. control, infarct + telomerase vs. control, and infarct + telomerase vs. infarct with the Linear Models for Microarray and RNA‑Seq Data package. Gene Ontology annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed for upregulated and downregulated genes by the Database for Annotation, Visualization and Integrated Discovery. Sub network modules of 3 protein‑protein interaction (PPI) networks were analyzed by Clustering with Overlapping Neighbourhood Expansion, and genes associated with telomerase were analyzed. Proto‑oncogene tyrosine‑protein kinase Src (Src) and proto‑oncogene tyrosine‑protein kinase Fyn (Fyn) were the hub nodes of the greatest degree in the PPI network for the infarct + telomerase vs. control comparison group and infarct + telomerase vs. infarct comparison group, respectively. Olfactory receptor gene family associated genes, including olfactory receptor 10 were significantly enriched in the sub network modules of the 3 comparison groups. In addition, olfactory transduction was a significantly enriched pathway by downregulation of DEGs in the infarct vs. control comparison group, and was additionally a significantly enriched pathway by upregulated DEGs in infarct + telomerase vs. infarct comparison group. Olfactory transduction was a significant pathway enriched by genes associated with telomerase. Telomerase activation may serve an important role in MI, in part, via the regulation of Src, Fyn and olfactory receptor family associated genes.