Abstract:
:Circular RNAs (circRNAs) are non-coding RNAs forming closed-loop structures, and their aberrant expression may lead to disease. However, the potential network of circRNA‑associated competing endogenous RNA (ceRNA) involved in nonvalvular persistent atrial fibrillation (NPAF) has not been previously reported. In the present study, four left atrial appendages (LAA) of patients with NPAF and four normal LAAs were examined via RNA sequencing, and their potential functions were investigated via bioinformatics analysis. The circRNA‑enriched genes were analyzed using Gene Ontology (GO) categories, while the enrichment of circRNAs was detected via the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. A total of 296 significantly dysregulated circRNA transcripts were obtained, with 238 upregulated and 58 downregulated. A number of circRNAs were further confirmed using reverse transcription‑quantitative polymerase chain reaction analysis. Furthermore, the more comprehensive circRNA‑associated ceRNA networks were examined in patients with NPAF. GO categories and KEGG annotation analysis of circRNAs revealed that the circRNA‑associated ceRNA networks were likely to influence AF though alterations in calcium and cardiac muscle contraction. The circRNA‑associated ceRNA networks revealed that dysregulated circRNAs in NPAF may be involved in regulating hsa‑microRNA (miR)‑208b and hsa‑miR‑21. To the best of our knowledge, this study presents the circRNA‑associated ceRNA networks in NPAF for the first time, which may have potential implications for the pathogenesis of AF. This study reveals a potential perspective from which to investigate circRNAs in circRNA‑associated ceRNA networks (hsa_circRNA002085, hsa_circRNA001321) in NPAF, and provides a potential biomarker for AF.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Zhang Y,Ke X,Liu J,Ma X,Liu Y,Liang D,Wang L,Guo C,Luo Ydoi
10.3892/mmr.2018.9695subject
Has Abstractpub_date
2019-01-01 00:00:00pages
638-650issue
1eissn
1791-2997issn
1791-3004journal_volume
19pub_type
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