Identification of potential novel biomarkers and therapeutic targets involved in human atrial fibrillation based on bioinformatics analysis.

BACKGROUND

Atrial fibrillation (AF) is the most common arrhythmia. However, exact molecular mechanism of AF remains unclear.

AIMS

Our study aimed to identify underlying biomarkers and pathways involved in AF based on bioinformatics analysis.

METHODS

The GSE79768 human heart tissue dataset was obtained from the Gene Expression Omnibus (GEO) database. A total of 26 heart tissue samples including 14 AF atrium heart tissue samples and 12 sinus rhythm heart tissue samples were used to identify the differentially expressed genes (DEGs). The functional enrichment analysis, protein‑protein interaction network, and miRNA-targeted gene regulatory network analysis were performed.

RESULTS

A total o f 260 DEGs were identified in the AF and sinus rhythm groups, including 150 up‑regulated and 110 down‑regulated genes. Functional and pathway enrichment analyses of DEGs indicated that they were mainly involved in inflammatory response, immune response, and receptor‑mediated endocytosis. In addition, CXCR4, CXCR2, C3, CXCL11, CCR2, AGTR2, CXCL1, and others were the hub nodes in the protein‑protein interaction network and module analysis revealed that these hub nodes were also significantly enriched in the inflammatory response, cytokine‑cytokine receptor interaction, chemokine signaling, and neuro‑active ligand‑receptor interaction pathways. Furthermore, miRNA‑targeted regulatory network analysis showed that 58 miRNA were involved in 61 regulatory relationships including 9 up‑regulated and 5 down‑regulated genes.

CONCLUSIONS

This study identified a series of key genes, including CXCR4, CXCR2, CXCL11, CCR2, LRRK2, IL1B, C3, CXCL1, and important miRNAs such as miR‑3123, miR‑548g‑3p, and miR‑9‑5p, along with pathways that were most closely related to human AF. Our results may provide a novel molecular mechanism and potential therapeutic targets for AF.