Reversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with

Yuk-Ling Dai1, Ting-Hin Luk, Kai-Hang Yiu

  • 1Cardiology Division, Department of Medicine, The University of Hong Kong, Hong Kong.

Atherosclerosis
|March 11, 2011
PubMed

Insights

Coenzyme Q10 (CoQ) supplementation improved mitochondrial function and endothelial function in patients with ischaemic left ventricular systolic dysfunction (LVSD). These improvements were linked, suggesting CoQ reverses mitochondrial dysfunction to enhance endothelial function.

Area of Science:

  • Cardiology
  • Biochemistry
  • Mitochondrial Medicine

Background:

  • Coronary artery disease (CAD) is linked to endothelial and mitochondrial dysfunction (MD).
  • Ischaemic left ventricular systolic dysfunction (LVSD) presents a significant clinical challenge.
  • Coenzyme Q10 (CoQ) is vital for mitochondrial energy production.

Purpose of the Study:

  • To evaluate CoQ supplementation's effect on MD and endothelial function in LVSD patients.
  • To determine if CoQ can reverse MD and improve endothelial function.

Main Methods:

  • A randomized, double-blind, placebo-controlled trial was conducted over 8 weeks.
  • CoQ (300 mg/day) or placebo was administered to patients with LVSD (ejection fraction <45%).
  • Brachial flow-mediated dilation (FMD) assessed endothelial function; plasma lactate/pyruvate ratio (LP ratio) indicated mitochondrial function.

Main Results:

  • CoQ treatment significantly increased plasma CoQ levels, improved FMD, and decreased LP ratio compared to placebo.
  • No significant changes were observed in blood pressure, glucose, lipids, or oxidative stress markers.
  • Reduced LP ratio positively correlated with improved FMD (r=-0.29, P=0.047).

Conclusions:

  • Eight weeks of CoQ supplementation improved mitochondrial function and FMD in ischaemic LVSD patients.
  • The correlation between FMD improvement and mitochondrial function suggests CoQ's mechanism involves reversing MD.
  • CoQ shows potential for improving endothelial function in LVSD by addressing mitochondrial dysfunction.
Abstract

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