Search

This study investigated the impact of resveratrol on abnormal metabolic remodeling in atrial fibrillation (AF) and explored potential molecular mechanisms. An AF cell model was established by high-frequency electrical stimulation of HL-1 atrial muscle cells. Resveratrol concentrations were optimized using CCK-8 and flow cytometry. AF-induced increases in ROS and mitochondrial calcium, along with decreased adenosine triphosphate (ATP) and mitochondrial membrane potential, were observed. Resveratrol mitigated these changes and maintained normal mitochondrial morphology. Moreover, resveratrol acted through the SIRT3-dependent pathway, as evidenced by its ability to suppress AF-induced acetylation of key metabolic enzymes. SIRT3 overexpression controls acetylation modifications, suggesting its regulatory role. In conclusion, resveratrol's SIRT3-dependent pathway intervenes in AF-induced mitochondrial dysfunction, presenting a potential therapeutic avenue for AF-related metabolic disorders. This study sheds light on the role of resveratrol in mitigating AF-induced mitochondrial remodeling and highlights its potential as a novel treatment for AF.

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.