Bioinformatics analysis to identify potential biomarkers and therapeutic targets for ST-segment-elevation myocardial infarction-related ischemic stroke.

Background: Acute myocardial infarction (AMI) is one of the major causes of mortality and disability worldwide, and ischemic stroke (IS) is a serious complication after AMI. In particular, patients with ST-segment-elevation myocardial infarction (STEMI) are more susceptible to IS. However, the interrelationship between the two disease mechanisms is not clear. Using bioinformatics tools, we investigated genes commonly expressed in patients with STEMI and IS to explore the relationship between these diseases, with the aim of uncovering the underlying biomarkers and therapeutic targets for STEMI-associated IS. Methods: Differentially expressed genes (DEGs) related to STEMI and IS were identified through bioinformatics analysis of the Gene Expression Omnibus (GEO) datasets GSE60993 and GSE16561, respectively. Thereafter, we assessed protein-protein interaction networks, gene ontology term annotations, and pathway enrichment for DEGs using various prediction and network analysis methods. The predicted miRNAs targeting the co-expressed STEMI- and IS-related DEGs were also evaluated. Results: We identified 210 and 29 DEGs in GSE60993 and GSE16561, respectively. CD8A, TLR2, TLR4, S100A12, and TREM1 were associated with STEMI, while the hubgenes, IL7R, CCR7, FCGR3B, CD79A, and ITK were implicated in IS. In addition, binding of the transcripts of the co-expressed DEGs MMP9, ARG1, CA4, CRISPLD2, S100A12, and GZMK to their corresponding predicted miRNAs, especially miR-654-5p, may be associated with STEMI-related IS. Conclusions: STEMI and IS are related and MMP9, ARG1, CA4, CRISPLD2, S100A12, and GZMK genes may be underlying biomarkers involved in STEMI-related IS.