Mitochondria-Targeted Antioxidant MitoQ 10 Improves Endothelial Function and Attenuates Cardiac Hypertrophy
Abstract
Mitochondria are a major site of reactive oxygen species production, which may contribute to the development of cardiovascular disease. Protecting mitochondria from oxidative damage should be an effective therapeutic strategy; however, conventional antioxidants are ineffective, because they cannot penetrate the mitochondria. This study investigated the role of mitochondrial oxidative stress during development of hypertension in the stroke-prone spontaneously hypertensive rat, using the mitochondria-targeted antioxidant, MitoQ 10 . Eight-week–old male stroke-prone spontaneously hypertensive rats were treated with MitoQ 10 (500 μmol/L; n=16), control compound decyltriphenylphosphonium (decylTPP; 500 μmol/L; n=8), or vehicle (n=9) in drinking water for 8 weeks. Systolic blood pressure was significantly reduced by ≈25 mm Hg over the 8-week MitoQ 10 treatment period compared with decylTPP (F=5.94; P =0.029) or untreated controls (F=65.6; P =0.0001). MitoQ 10 treatment significantly improved thoracic aorta NO bioavailability (1.16±0.03 g/g; P =0.002, area under the curve) compared with both untreated controls (0.68±0.02 g/g) and decylTPP-treated rats (0.60±0.06 g/g). Cardiac hypertrophy was significantly reduced by MitoQ 10 treatment compared with untreated control and decylTPP treatment (MitoQ 10 : 4.01±0.05 mg/g; control: 4.42±0.11 mg/g; and decylTPP: 4.40±0.09 mg/g; ANOVA P =0.002). Total MitoQ 10 content was measured in liver, heart, carotid artery, and kidney harvested from MitoQ 10 -treated rats by liquid chromatography-tandem mass spectrometry. All of the organs analyzed demonstrated detectable levels of MitoQ 10 , with comparable accumulation in vascular and cardiac tissues. Administration of the mitochondria-targeted antioxidant MitoQ 10 protects against the development of hypertension, improves endothelial function, and reduces cardiac hypertrophy in young stroke-prone spontaneously hypertensive rats. MitoQ 10 provides a novel approach to attenuate mitochondrial-specific oxidative damage with the potential to become a new therapeutic intervention in human cardiovascular disease.
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When MitoQ is administered to in vivo animal models of pathologies, it reduces both oxidative damage and the pathologies.
“A number of studies show that, when MitoQ is administered to in vivo animal models of pathologies, it reduces both oxidative damage and the pathologies (Adlam et al., 2005; Lowes et al., 2008; Graham et al., 2009; Supinski et al., 2009; Chacko et al., 2010; Smith and Murphy 2010).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Graham et al., 2009
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Mitochondria and Endothelial Function
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Retracted
- Authors
- Graham, D., Huynh, N. N., Hamilton, C. A., Beattie, E., Smith, R. A. J., Cochemé, H. M., Murphy, M. P., & Dominiczak, A. F.
- Affiliations
- British Heart Foundation (GB)
- From the British Heart Foundation Glasgow Cardiovascular Research Centre (D.G., N.N.H., C.A.H., E.B., A.F.D.), Faculty of Medicine, University of Glasgow, Glasgow, United Kingdom; Department of Chemistry (R.A.J.S.), University of Otago, Dunedin, New Zealand; Medical Research Council Mitochondrial Biology Unit (H.M.C., M.P.M.), Cambridge, United Kingdom.
- Venue
- Hypertension
- Published
- 2009-08
- Volume
- 54
- Issue
- 2
- Pages
- 322-328
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2123051296
- Cited by
- 367
- References
- 8
- Citations by year
- 2026: 16 · 2025: 20 · 2024: 16 · 2023: 26 · 2022: 24 · 2021: 26 · 2020: 22 · 2019: 14 · 2018: 27 · 2017: 17 · 2016: 23 · 2015: 15 · 2014: 27 · 2013: 23 · 2012: 21
- FWCI
- 14.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Wellcome Trust
- British Heart Foundation
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- mitochondria-targeted antioxidants, mitochondrial oxidative stress, endothelial function, cardiac hypertrophy, stroke-prone spontaneously hypertensive rats, nitric oxide bioavailability, reactive oxygen species, mitochondrial accumulation, blood pressure reduction, cardiovascular disease prevention, mitochondria-targeted drug delivery
- MeSH terms
- Analysis of Variance, Animals, Antioxidants, Blood Pressure, Disease Models, Animal, Endothelium, Vascular, Cardiomegaly, Hypertension, Male, Mitochondria, Probability, Random Allocation, Rats, Inbred SHR, Risk Factors, Sensitivity and Specificity, Ubiquinone, Drug Delivery Systems, Oxidative Stress, Rats, Membrane Potential, Mitochondrial
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