Circulating miR-106a may Function as Potential Biomarkers in Patients with Coronary Artery Disease

Clinical Laboratory
|October 19, 2019
PubMed

Insights

Plasma miR-106a levels are elevated in coronary artery disease (CAD) patients, indicating its potential as a biomarker for early diagnosis and assessing disease severity. This finding aids in understanding CAD progression.

Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Molecular Biology

Background:

  • Coronary artery disease (CAD) is a leading cause of cardiovascular mortality and sudden cardiac death.
  • Early diagnosis and identification of novel biomarkers are crucial for managing CAD.
  • This study investigates the role of microRNA-106a (miR-106a) as a potential biomarker in CAD.

Purpose of the Study:

  • To determine the clinical significance of plasma miR-106a levels in patients with CAD.
  • To assess the correlation between plasma miR-106a levels and CAD severity (SYNTAX score).
  • To explore the relationship between miR-106a, oxidized low-density lipoprotein (ox-LDL), and 25-hydroxyvitamin D3 (25(OH)D3) in CAD patients.

Main Methods:

  • Plasma samples from 92 CAD patients and 92 healthy controls were analyzed.
  • Quantitative real-time PCR (RT-qPCR) was used to measure miR-106a expression levels.
  • Associations with SYNTAX score, ox-LDL, and 25(OH)D3 levels were statistically analyzed.

Main Results:

  • miR-106a was significantly upregulated in the plasma of CAD patients compared to controls.
  • Receiver operating characteristic (ROC) curve analysis indicated miR-106a as a sensitive diagnostic biomarker for CAD (AUC = 0.8189).
  • Plasma miR-106a levels positively correlated with SYNTAX score, ox-LDL levels, and negatively correlated with 25(OH)D3 levels.

Conclusions:

  • miR-106a is upregulated in CAD and shows potential as a biomarker for early diagnosis.
  • Plasma miR-106a levels may aid in evaluating the clinical outcomes and severity of CAD.
  • The findings suggest a link between miR-106a, lipid metabolism, and vitamin D status in CAD pathogenesis.
Abstract

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