Identifying the key microRNAs implicated in atrial fibrillation

识别与心房颤动相关的关键microRNA

阅读:1

Abstract

OBJECTIVE: This study investigated the potential microRNAs (miRNAs) having a diagnostic value in atrial fibrillation (AF). METHODS: The miRNA and mRNA expression profiles of atrial tissue from healthy individuals and patients with AF were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs/mRNAs (DEMis/DEMs) were identified in patients with AF. Furthermore, an interaction network between DEMis and DMEs was constructed. The biological processes, molecular functions, and signaling pathways of DEMs were enriched. Then, the diagnostic values of candidate DECs among healthy individuals and patients with AF were preliminarily evaluated in the GSE101586, GSEE101684, and GSE112214 datasets. RESULTS: Twenty DEMis were identified in patients with AF, including seven upregulated and 13 downregulated DEMis. Furthermore, 2,307 DEMs were identified in patients with AF. In the DEMi-DEM interaction network, downregulated miR-193b and upregulated miR-16 interacted with the most targeted DEMs, which interacted with 72 and 65 targeted DEMs, respectively. The targeted DEMs were significantly enriched in biological functions including apoptosis and the PI3K-Akt, mTOR, Hippo, HIF-1, and ErbB signaling pathways. Four of the 20 DEMis (i.e., miR-490-3p, miR-630, miR-146b-5p, and miR-367) had a potential value to distinguish patients with AF from healthy individuals in the GSE68475, GSE70887, and GSE28954 datasets. The area under the curve values for those four DEMis were 0.751, 0.719, 0.709, and 0.7, respectively. CONCLUSION: DEMis might play key roles in AF progression through the mTOR and Hippo signaling pathways. miR-409-3p, miR-630, miR-146b-5p, and miR-367 had a potential diagnostic value to discriminate patients with AF from healthy controls in this study.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。