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Related Experiment Video

Updated: Jun 25, 2025

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Circ_0000006 and circ_0000160 regulate hsa-let-7e-5p/UBQLN4 axis in aortic dissection progression.

Yong Liu1, Liang Wang1, Dongyun Lei2

  • 1Department of Cardiovascular Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, China.

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|May 31, 2024
PubMed
Summary

Circular RNAs (circRNAs) circ_0000006 and circ_0000160 promote aortic dissection (AD) progression by affecting vascular smooth muscle cells. Targeting these circRNAs may offer a therapeutic strategy for AD.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Aortic aneurysms (AA) and aortic dissection (AD) are critical vascular conditions with increasing incidence and mortality.
  • Non-coding RNAs, including circRNAs and microRNAs (miRNAs), are implicated in the pathogenesis of AA and AD.

Purpose of the Study:

  • To identify the circRNA-miRNA-mRNA axis regulating the transition from AA to AD.
  • To investigate the functional roles of key molecules in AD development.

Main Methods:

  • Plasma samples from AA and AD patients underwent circRNA, miRNA, and mRNA sequencing.
  • In vitro studies utilized an AD cell model with vascular smooth muscle cells (VSMCs).
  • In vivo studies employed an animal model of AD.

Main Results:

  • Elevated circ_0000006 and circ_0000160, with decreased hsa-let-7e-5p, were observed in AD samples.
  • circ_0000006 and circ_0000160 silencing attenuated PDGF-induced VSMC changes; this was partially reversed by hsa-let-7e-5p inhibition.
  • Overexpression of Ubiquilin 4 (UBQLN4) counteracted hsa-let-7e-5p effects, indicating UBQLN4 as a downstream mediator.
  • Knockdown of circ_0000006 and circ_0000160 demonstrated protective effects in an animal AD model.

Conclusions:

  • Upregulated circ_0000006 and circ_0000160 contribute to AA to AD progression via VSMC dysfunction.
  • The hsa-let-7e-5p/UBQLN4 axis is crucial in AD pathogenesis.
  • Targeting circ_0000006 and circ_0000160 presents a potential therapeutic avenue for AD prevention.