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Updated: Jun 3, 2026

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
Published on: June 1, 2022
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.
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.
Aims:
Coronary artery disease (CAD) is associated with endothelial dysfunction and mitochondrial dysfunction (MD). The aim of this study was to investigate whether co-enzyme Q10 (CoQ) supplementation, which is an obligatory coenzyme in the mitochondrial respiratory transport chain, can reverse MD and improve endothelial function in patients with ischaemic left ventricular systolic dysfunction (LVSD).
Methods And Results:
We performed a randomized, double-blind, placebo-controlled trial to determine the effects of CoQ supplement (300 mg/day, n=28) vs. placebo (controls, n=28) for 8 weeks on brachial flow-mediated dilation (FMD) in patients with ischaemic LVSD(left ventricular ejection fraction <45%). Mitochondrial function was determined by plasma lactate/pyruvate ratio (LP ratio). After 8 weeks, CoQ-treated patients had significant increases in plasma CoQ concentration (treatment effect 2.20 μg/mL, P<0.001) and FMD (treatment effect 1.51%, P=0.03); and decrease in LP ratio (treatment effect -2.46, P=0.03) compared with controls. However, CoQ treatment did not alter nitroglycerin-mediated dilation, blood pressure, blood levels of fasting glucose, haemoglobin A1c, lipid profile, high-sensitivity C-reactive protein and oxidative stress as determined by serum superoxide dismutase and 8-isoprostane (all P>0.05). Furthermore, the reduction in LP ratio significantly correlated with improvement in FMD (r=-0.29, P=0.047).
Conclusion:
In patients with ischaemic LVSD, 8 weeks supplement of CoQ improved mitochondrial function and FMD; and the improvement of FMD correlated with the change in mitochondrial function, suggesting that CoQ improved endothelial function via reversal of mitochondrial dysfunction in patients with ischaemic LVSD.
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