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Updated: Jul 30, 2025

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
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Construction and integrated analysis of the ceRNA network hsa_circ_0000672/miR-516a-5p/TRAF6 and its potential

Xing Liu1,2, Mingxing Wu1, Yan He2

  • 1Department of Cardiology, Xiangtan Central Hospital, Xiangtan, China.

Scientific Reports
|May 11, 2023
PubMed

Insights

Atrial fibrosis, a key factor in atrial fibrillation (AF), is linked to a specific circRNA network. Elevated hsa_circ_0000672 in AF patients may indicate fibrosis, potentially via the hsa_circ_0000672/hsa_miR-516a-5p/TRAF6 axis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Biomedical Engineering

Background:

  • Atrial fibrosis significantly contributes to the initiation and progression of atrial fibrillation (AF).
  • Understanding the molecular mechanisms underlying atrial fibrosis is crucial for developing targeted therapies for AF.
  • Circular RNAs (circRNAs) are emerging as key regulators in various biological processes, including cardiac remodeling.

Purpose of the Study:

  • To identify a circRNA-miRNA-mRNA competitive endogenous RNA (ceRNA) regulatory network associated with atrial fibrosis in AF.
  • To specifically validate the hsa_circ_0000672/hsa_miR-516a-5p/TRAF6 ceRNA axis in the context of AF-related fibrosis.

Main Methods:

  • Construction of a ceRNA network using bioinformatic tools and literature review.
  • Assessment of left atrium (LA) fibrosis by LA low voltage mapping.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) to measure gene expression in peripheral blood monocytes.
  • Dual-luciferase reporter assay to confirm the interaction between circRNA, miRNA, and target gene.

Main Results:

  • A ceRNA network was constructed, involving up-regulated hsa_circ_0000672 and hsa_circ_0003916, down-regulated miR-516a-5p, and up-regulated hub genes (KRAS, SMAD2, TRAF6, MAPK11, SMURF1).
  • Hub genes were significantly enriched in TGF-beta and MAPK signaling pathways.
  • Hsa_circ_0000672 expression was significantly higher in peripheral blood monocytes of persistent AF patients compared to controls, and even higher in those with LA low voltage (fibrosis).
  • Dual-luciferase assay confirmed hsa_circ_0000672 acts as a sponge for miR-516a-5p, regulating TRAF6 expression.

Conclusions:

  • Hsa_circ_0000672 expression in peripheral blood monocytes may serve as a potential biomarker for atrial fibrosis in AF.
  • The identified hsa_circ_0000672/hsa_miR-516a-5p/TRAF6 axis is preliminarily validated and may play a role in atrial fibrosis pathogenesis.
  • This study provides insights into the molecular mechanisms of atrial fibrosis and suggests potential therapeutic targets for AF.

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