Differential Expression of Peripheral Circulating MicroRNA-146a Between Patients with Atherosclerotic Vulnerable

Yenwen Song1, Lei Zhang1, Ye Huang1

  • 1Department of Emergency, Xiyuan Hospital, Chinese Academy of Traditional Chinese Medicine.

PubMed

Insights

Circulating microRNA-146a (miR-146a) levels are significantly higher in patients with vulnerable atherosclerotic plaques compared to stable plaques. This finding suggests miR-146a may serve as a potential biomarker for plaque vulnerability.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Biomarker Discovery

Background:

  • Atherosclerotic plaque rupture is a major cause of cardiovascular disease.
  • MicroRNA-146a (miR-146a) polymorphism is linked to plaque vulnerability.
  • The role of circulating miR-146a levels in differentiating stable from vulnerable plaques is unclear.

Purpose of the Study:

  • To investigate differential expression of circulating miR-146a between stable and vulnerable atherosclerotic plaques.
  • To explore miR-146a's potential as a biomarker for plaque vulnerability.
  • To analyze potential molecular mechanisms involving miR-146a.

Main Methods:

  • Systematic review and meta-analysis of published studies up to November 2022.
  • Inclusion of studies reporting circulating miR-146a levels in stable vs. vulnerable plaque patients.
  • Quality assessment using the modified Newcastle-Ottawa scale and meta-analysis of standardized mean difference (SMD).

Main Results:

  • Eight studies with 978 patients were analyzed.
  • Circulating miR-146a levels were significantly higher in the vulnerable plaque group (SMD: 1.91, P < 0.01).
  • Subgroup analyses and sensitivity analyses confirmed the robustness of these findings.

Conclusions:

  • Patients with vulnerable atherosclerotic plaques exhibit elevated circulating miR-146a levels compared to those with stable plaques.
  • miR-146a may be a potential biomarker for identifying vulnerable plaques.
  • Further high-quality studies are needed to validate these findings and elucidate underlying mechanisms, possibly involving ACTN4, SARM1, and ULK2 regulation.

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