Research
Mitoq
22 peer-reviewed studies curated from PubMed and Semantic Scholar.
Studies
Sorted by quality and recency
Overview of MitoQ on prevention and management of cardiometabolic diseases: a scoping review.
This scoping review synthesizes current research on the health impacts of MitoQ on cardiometabolic diseases, focusing primarily on human-based clinical trials. The review highlights benefits such as enhanced insulin secretion, improved lipid profiles, and mitochondrial function, but notes the need for further investigation on appropriate doses and populations.
Effects of Mitoquinone (MitoQ) Supplementation on Aerobic Exercise Performance and Oxidative Damage: A Systematic Review and Meta-analysis.
Systematic review and meta-analysis of eight studies with 188 subjects assessing MitoQ supplementation on aerobic exercise performance and oxidative damage. MitoQ effectively reduces exercise-induced oxidative damage but does not improve endurance exercise performance. MitoQ may improve exercise tolerance in subjects with peripheral artery disease.
Effect of Combined Endurance Training and MitoQ on Cardiac Function and Serum Level of Antioxidants, NO, miR-126, and miR-27a in Hypertensive Individuals.
Double-blind randomized clinical trial with 52 male hypertensive participants assessing the effects of MitoQ supplementation and endurance training, alone and in combination, on cardiac function and serum biomarkers. The combination of MitoQ and endurance training showed significant improvements in systolic and diastolic blood pressure, left ventricular hypertrophy, and serum antioxidant levels, with modulation of miR-126 and miR-27a.
The Effect of MitoQ on Aging-Related Biomarkers: A Systematic Review and Meta-Analysis.
Systematic review and meta-analysis investigating the effects of MitoQ on oxidative outcomes related to aging. MitoQ intervention produced a statistically significant reduction in nitrotyrosine concentration and increased membrane potential, suggesting potential benefits in alleviating oxidative stress related to aging.
Translational studies of chronic supplementation with a mitochondria-targeted antioxidant to improve physical function with ageing.
The study investigated the effects of the mitochondria-targeted antioxidant MitoQ on physical function in ageing. In old mice, MitoQ improved grip strength, coordination, and endurance, accompanied by reduced mitochondrial oxidative stress and inflammation. In a clinical trial with older adults, no convincing effects were observed, though exploratory analyses suggested potential benefits in participants aged ≥70 years.
A pilot double-blind, placebo-controlled, randomized clinical trial of MitoQ in the treatment of septic shock: evaluating its effects on clinical outcomes and oxidative stress biomarker.
This pilot RCT investigated mitoquinone mesylate (MitoQ) in septic shock patients, focusing on clinical outcomes and oxidative stress biomarkers. MitoQ improved oxidative biomarkers significantly at day 5 compared to placebo, but its impact on clinical outcomes like 28-day mortality and organ recovery was not significant.
MitoQ supplementation does not impact redox responses to acute exercise in skeletal muscle of older individuals.
RCT investigating the effects of MitoQ supplementation on mitochondrial bioenergetics and redox responses to acute exercise in skeletal muscle of older individuals. MitoQ reduced mitochondrial HOemission capacity but did not impact mitochondrial respiration or redox responses to exercise.
Acute effects of MitoQ on vascular endothelial function are influenced by cardiorespiratory fitness and baseline FMD in middle-aged and older adults.
A double-blind, randomized, placebo-controlled crossover study with 23 middle-aged and older adults examined the effects of a single dose of mitoquinone mesylate (MitoQ) on vascular endothelial function. MitoQ increased flow-mediated dilatation (FMD) in non-exercisers and those with baseline FMD <6%, but not in exercisers or those with higher baseline FMD.
Acute high-dose MitoQ does not increase urinary kidney injury markers in healthy adults: a randomized crossover trial.
Randomized crossover trial in 32 healthy adults assessing the effect of acute high-dose MitoQ on urinary kidney injury markers. The study found that MitoQ supplementation did not influence urine flow rate, creatinine clearance, or urinary kidney injury markers, suggesting it is not nephrotoxic in healthy adults.
Chronic mitochondria antioxidant treatment in older adults alters the circulating milieu to improve endothelial cell function and mitochondrial oxidative stress.
A crossover, placebo-controlled clinical trial in older adults showed that 6 weeks of MitoQ supplementation improved endothelial function by lowering mitochondrial oxidative stress and reducing circulating oxidized low-density lipoprotein levels. The study found that MitoQ enhanced nitric oxide production and reduced mitochondrial oxidative stress in endothelial cells.
Effects of a mitochondrial-targeted ubiquinol on vascular function and exercise capacity in chronic kidney disease: a randomized controlled pilot study.
This randomized controlled pilot study investigated the effects of mitochondria-targeted ubiquinol (MitoQ) on vascular function and exercise capacity in 18 patients with chronic kidney disease. MitoQ improved macrovascular endothelial function, arterial hemodynamics, and microvascular function but did not affect exercise capacity.
Mitochondrial-targeted antioxidant ingestion acutely blunts VOin physically inactive females.
RCT with 9 physically inactive females examining the acute effects of MitoQ on metabolic response during exercise. MitoQ ingestion resulted in lower VO2 and maximal ventilation compared to placebo, suggesting that mitochondrial reactive oxygen species are necessary for maximal aerobic capacity.
Mitochondria-targeted antioxidant supplementation does not affect muscle soreness or recovery of maximal voluntary isometric contraction force following muscle-damaging exercise in untrained men: a randomized clinical trial.
RCT of 32 untrained men examining the effect of MitoQ supplementation on muscle recovery following eccentric exercise. MitoQ did not affect muscle soreness or recovery of maximal voluntary isometric contraction force, and delayed recovery of peak eccentric torque.
MitoQ supplementation augments acute exercise-induced increases in muscle PGC1α mRNA and improves training-induced increases in peak power independent of mitochondrial content and function in untrained middle-aged men.
RCT investigating the effect of MitoQ supplementation on muscle adaptations to exercise in 23 untrained middle-aged men. MitoQ augmented acute exercise-induced increases in muscle PGC1α mRNA and improved training-induced increases in peak power, independent of mitochondrial content and function.
Mitochondria-targeted antioxidant supplementation improves 8 km time trial performance in middle-aged trained male cyclists.
A randomized, double-blind, placebo-controlled crossover study investigated the effects of MitoQ supplementation on cycling performance in 19 middle-aged trained male cyclists. MitoQ supplementation resulted in a 1.3% faster 8 km time trial completion time and a 4.4% increase in average power output compared to placebo. Plasma F-isoprostanes were lower following MitoQ supplementation, suggesting reduced oxidative damage.
The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage.
Double-blind, randomized, placebo-controlled trial with 24 healthy male participants examining the effects of MitoQ on exercise-induced mitochondrial DNA damage. Chronic MitoQ supplementation attenuated nuclear and mtDNA damage in lymphocytes and muscle tissue, suggesting a protective effect on genome stability.
Acute mitochondrial antioxidant intake improves endothelial function, antioxidant enzyme activity, and exercise tolerance in patients with peripheral artery disease.
This randomized crossover study investigated the effects of acute MitoQ intake on endothelial function, antioxidant enzyme activity, and exercise tolerance in 11 patients with peripheral artery disease (PAD). MitoQ intake improved brachial and popliteal artery flow-mediated dilation, superoxide dismutase activity, maximal walking time, and claudication onset time, suggesting benefits for vascular function and exercise capacity in PAD patients.
Mitochondria-specific antioxidant supplementation does not influence endurance exercise training-induced adaptations in circulating angiogenic cells, skeletal muscle oxidative capacity or maximal oxygen uptake.
RCT investigating the effects of MitoQ supplementation on endurance exercise training adaptations in young healthy men. MitoQ did not alter increases in circulating angiogenic cells, muscle mitochondrial capacity, or maximal oxygen uptake induced by exercise training.
A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson's disease.
Double-blind, placebo-controlled study of MitoQ in 128 newly diagnosed untreated Parkinson's disease patients over 12 months. MitoQ showed no difference from placebo in slowing PD progression as measured by clinical scores.
Chronic Supplementation With a Mitochondrial Antioxidant (MitoQ) Improves Vascular Function in Healthy Older Adults.
RCT of 20 healthy older adults with impaired endothelial function, testing 6 weeks of oral MitoQ supplementation versus placebo. MitoQ improved vascular endothelial function, reduced aortic stiffness, and lowered plasma oxidized LDL, suggesting potential benefits for age-related vascular dysfunction.
Redox-crippled MitoQ potently inhibits breast cancer and glioma cell proliferation: A negative control for verifying the antioxidant mechanism of MitoQ in cancer and other oxidative pathologies
The study investigates the antiproliferative effects of MitoQ and its modified form, DM-MitoQ, on breast cancer and glioma cells. MitoQ, a mitochondria-targeted coenzyme Q10, inhibited tumor growth and cell proliferation, while DM-MitoQ, lacking antioxidant function, was slightly more potent in inhibiting cell proliferation. Both compounds inhibited mitochondrial complex I-dependent oxygen consumption.
Treating the placenta to prevent adverse effects of gestational hypoxia on fetal brain development
The study investigated the effects of gestational hypoxia on fetal brain development and whether the mitochondria-targeted antioxidant MitoQ could prevent these effects. Gestational hypoxia caused low birth-weight and brain changes in offspring, similar to those seen in neuropsychiatric diseases. MitoQ, when bound to nanoparticles, prevented oxidative stress in the placenta and associated molecular and morphological changes.