Background Being the most common arrhythmia in clinic, atrial fibrillation (AF) causes various comorbidities to patients such as heart failure and stroke. LncRNAs were reported involved in pathogenesis of AF, yet, little is known about AF-associated lncRNAs. The present study aims to explore lncRNAs associated with AF susceptibility based on competing endogenous RNA (ceRNA) network analysis and weighted gene co-expression network analysis (WGCNA). Methods GSE41177 and GSE79768 datasets were obtained from the Gene Expression Omnibus (GEO) database. Competing endogenous RNA (ceRNA) network analysis was performed using GSE41177. Differentially expressed lncRNAs (DElncRNAs), mRNAs (DEmRNAs) between AF patients and patients with sinus rhythm (SR) were identified from GSE41177 using R software. Then, the ceRNA network was constructed based on DElncRNAs, the predicted target miRNAs and DEmRNAs. Weighted gene co-expression network analysis (WGCNA) was performed using GSE79768 to validate the AF-related lncRNAs identified from GSE41177. LncRNA modules and crucial lncRNAs relevant to AF and were identified. Results In summary, 18 DElncRNAs and 350 DEmRNAs were found between AF patients and SR patients. A total of 5 lncRNAs, 10 miRNAs, and 21 mRNAs were contained in the final ceRNA network. Taking into consideration both the ceRNA theory and inference scores from the comparative toxicogenomics database (CTD) database, the ceRNA axis FAM201A-miR-33a-3p-RAC3 was identified as mostly relevant to AF susceptibility. FAM201A (Gene significance, GS = − 0.62; Module membership, MM = 0.75) was also proved in the blue module, which was identified most highly relevant with AF by WGCNA. Conclusions These results demonstrated that decreased expression of FAM201A might be associated with susceptibility of AF. Working as the ceRNA to regulate RAC3 might be one function of FAM201A in AF susceptibility, which requires further exploration in future research.

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia that contributes to various complications. However, little is known about lncRNAs associated with AF susceptibility. In the present study, we aim to identify lncRNAs involved in pathogenesis of AF based on competing endogenous RNA (ceRNA) network analyses and weighted gene co-expression network analysis (WGCNA).Methods: Two lncRNA and mRNA microarray datasets GSE41177 and GSE79768 were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed lncRNAs (DElncRNAs), mRNAs (DEmRNAs) between AF patients and patients with sinus rhythm (SR) were identified from dataset GSE41177. Then, those DElncRNAs associated target miRNAs were predicted. The ceRNA network was constructed based on DElncRNAs, predicted miRNAs and DEmRNAs. To validate the role of AF-related lncRNAs, all lncRNAs form dataset GSE79768 were selected to perform WGCNA. LncRNA modules relevant to AF were identified. Crucial lncRNAs in the module that was most relevant to AF were screened according to the criteria of | Gene significance (GS)| > 0.6 and |Module membership (MM)| > 0.5. Results: A total of 18 DElncRNAs and 350 DEmRNAs were identified between AF patients and SR patients. The final ceRNA network contained 5 lncRNAs, 10 miRNAs, and 21 mRNAs. According to the ceRNA theory, combined with the comparative toxicogenomics database (CTD) database, the ceRNA axis FAM201A-miR-33a-3p-RAC3 was considered associated with AF susceptibility. By WGCNA, the blue module was detected most highly relevant with AF. The lncRNA FAM201A was proved in the blue module and highly related to AF. Conclusions: These results demonstrated that FAM201A might have great potential for susceptibility of AF based on ceRNA network analyses and WGCNA. FAM201A may function, at least partly, as ceRNA to regulate RAC3 in AF susceptibility.