BACKGROUND: Atrial fibrillation (AF) is a highly prevalent condition associated with high morbidity and mortality that can cause or exacerbate heart failure and is an important risk factor for stroke. AF is the disorganized propagation of electrical activity in the atrium, which prevents organized contractions. However, the effect of microRNAs and the patterns of the regulatory network of AF remain vague.

MATERIAL AND METHODS: The mRNA expression data of atrial tissue splices from 3 conditions – permanent atrial fibrillation (AF), sinus rhythm (SR), and human left ventricular non-failing myocardium (LV) – were downloaded from GSE2240 and the differentially expressed genes (DEGs) between the 3 kinds of samples were calculated. Then we constructed 3 miRNA-DEGs networks and these networks were integrated to construct the final merged AF-related microRNA regulatory network. Finally, we constructed the miRNA-inflammation networks to detect the roles of miRNAs in inflammation development of AF.

RESULTS: This network included 108 DEGs, and 27 microRNAs and DEGs are regulated by both microRNAs. We found that a sub-network composed by miR-124, miR-183, miR-215, miR-192, and a DEG of EGR1 were all represents in these 3 networks. Based on functional enrichment analysis, some biological process, such as energy and glucan metabolic process and heart and blood vessel development, were found to be regulated by miRNAs in AF. Some miRNAs, such as miR-26b and miR-355p, were involved in inflammation in AF.

CONCLUSIONS: In conclusion, the microRNA regulatory network sheds new light on the molecular mechanism of AF with this non-coding regulated model.

Keywords: Atrial Fibrillation - pathology, Databases, Genetic, Gene Regulatory Networks, Heart Atria - physiopathology, Inflammation - pathology, Myocardium - pathology