OBJECTIVE: Atrial fibrillation (AF) is the most common type of arrhythmia, especially in rheumatic heart disease (RHD) patients. The differences in structural remodeling and electrical remodeling between the left and right atrium associated with AF in RHD patients are well known, and alterations in the expression profiles of long noncoding RNAs (lncRNAs) in the left atrium have also been investigated. However, the role of lncRNAs in the right atrium (RA) remains largely unknown. PATIENTS AND METHODS: We identified differentially expressed lncRNAs in RA tissues of RHD patients with AF or a normal sinus rhythm (NSR) using microarray analysis. Then, we performed gene ontology (GO) and KEGG pathway analyses for functional annotation of the deregulated lncRNAs. Finally, we constructed a lncRNA-mRNA co-expression network. RESULTS: Of the 22,829 human non-coding RNAs analyzed, a total of 1,909 long non-coding RNAs were detected. A total of 182 lncRNAs (117 downregulated and 65 upregulated) were shown to be differentially expressed (fold-change > 1.5) in AF patients compared with NSR patients. Many lncRNAs might be partially involved in an AF-related pathway. CONCLUSIONS: AF dysregulates the expression of lncRNAs in the RA of RHD patients. These findings may be useful for exploring potential therapeutic treatments for AF in RHD patients.
OBJECTIVE:Atrial fibrillation (AF) is the most common type of arrhythmia, especially in rheumatic heart disease (RHD) patients. The differences in structural remodeling and electrical remodeling between the left and right atrium associated with AF in RHD patients are well known, and alterations in the expression profiles of long noncoding RNAs (lncRNAs) in the left atrium have also been investigated. However, the role of lncRNAs in the right atrium (RA) remains largely unknown. PATIENTS AND METHODS: We identified differentially expressed lncRNAs in RA tissues of RHD patients with AF or a normal sinus rhythm (NSR) using microarray analysis. Then, we performed gene ontology (GO) and KEGG pathway analyses for functional annotation of the deregulated lncRNAs. Finally, we constructed a lncRNA-mRNA co-expression network. RESULTS: Of the 22,829 human non-coding RNAs analyzed, a total of 1,909 long non-coding RNAs were detected. A total of 182 lncRNAs (117 downregulated and 65 upregulated) were shown to be differentially expressed (fold-change > 1.5) in AFpatients compared with NSR patients. Many lncRNAs might be partially involved in an AF-related pathway. CONCLUSIONS:AF dysregulates the expression of lncRNAs in the RA of RHD patients. These findings may be useful for exploring potential therapeutic treatments for AF in RHD patients.