Founded in science, studied around the world, clinically tested.

MitoQ encourages the scientific community to explore and discover the benefits of our ingredient Mitoquinol Mesylate.


19 clinical trials, 750+ peer-reviewed scientific papers, and over $60 million invested in a broad range of independent studies.


Harvard University, UCLA, University of Cambridge and more leading institutions around the world have studied MitoQ’s cellular health optimization.


Our product development team continues to explore the leading edge of cellular health science, resulting in over 60 global patents for our molecular technology.

Meet our MitoQ science experts

a headshot of Professor Mike Murphy in cell shape


Ph.D., MitoQ co-founder and Professor of Mitochondrial Redox Biology at the University of Cambridge

a headshot of Dr Richard Siow in cell shape


Ph.D., Director of Ageing Research at King’s College London, Honorary Secretary General of European Society of Preventive Medicine

a headshot of Professor Marcia Haigis in cell shape


Ph.D., Professor of Cell Biology at Harvard Medical School, National Academy of Medicine's Emerging Leader in Health and Medicine

a headshot of Professor Doug Seals in cell shape


Ph.D., Professor in Integrative Physiology at the University of Colorado Boulder

a headshot of Dr Molly Maloof in cell shape


M.D., author, entrepreneur, lecturer, medical advisor

Kaytee Boyd


BSC, B PHED, CHEK HLC II, Integrative nutritionist

750+ independent high-impact, peer-reviewed journals, and 19 clinical trials. Here are some highlights.


Chronic supplementation with a mitochondrial antioxidant (MitoQ) improves vascular function in healthy older adults

Rossman MJ et al. Hypertension. 71:1056-1063 (2018)

DOI: DOI: 10.1161/HYPERTENSIONAHA.117.10787 source

MitoQ decreases free radical production by mitochondria, and significantly supports arterial function in older adults and therefore the health of the arteries. In this clinical trial it was confirmed that: MitoQ greatly improved the ability of arteries to dilate (by 42%). MitoQ significantly supports the health of aorta and factors related to heart lipid metabolism.

Read the summary


The mitochondria-targeted antioxidant MitoQ, attenuates exercise-induced mitochondrial DNA damage

Williamson et al. REDOX Biology

DOI: DOI: 10.1016/j.redox.2020.101673 Source

High-intensity exercise increases our respiration rate and can lead to oxidative stress. The free radicals that are produced during exercise are known to damage our DNA. This study showed that after 3 weeks of chronic supplementation, 20 mg/day of MitoQ was able to protect against exercise-induced DNA damage in young healthy men (20-30 years old). MitoQ significantly reduced both nuclear and mitochondrial DNA damage in the blood and in muscle tissue after intense exercise.

Read the study


Mitochondria-targeted antioxidant supplementation improves 8km time trial performance in middle-aged trained male cyclist

Broome SC et al. J. Int. Soc. Sports Nutr. 18, 58 (2021).

DOI: DOI: 10.1186/s12970-021-00454-0 source

The study showed that after 4 weeks of MitoQ supplementation, the mean completion time for a time trial was 10.8 seconds faster and an increase of 10 watts of power. MitoQ supplementation may be an effective nutritional strategy to attenuate exercise-induced increases in oxidative damage to lipids and improve cycling performance.

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The influence of acute high dose MitoQ on urinary kidney injury markers in healthy adults

Linder BA et al. The FASEB Journal. 36, S1 (2022).

DOI: DOI: 10.1096/fasebj.2022.36.S1.L7715 source

Results found that acute, high-dose MitoQ supplementation did not result in high concentrations of kidney injury biomarkers compared to placebo samples. Preliminary evidence is that ongoing MitoQ use in the normal range (10mg-20mg) supports kidney health.

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MitoQ and CoQ10 supplementation mildly suppresses skeletal muscle mitochondrial hydrogen peroxide levels without impacting mitochondrial function in middle‑aged men

Pham et al. European Journal of Applied Physiology

DOI: DOI: 10.1007/s00421-020-04396-4 Source

Mitochondria are the main source of oxidative stress in our bodies. Oxidative stress is caused by an imbalance of free radicals and our levels of antioxidants. Over time, oxidative stress can lead to cell damage and have flow-on effects for our health. This study compared the effects of 20 mg/day MitoQ and 200 mg/day CoQ10 on biomarkers of mitochondrial health and oxidative stress in healthy middle-aged men (40-60 years old). After six weeks of supplementation, MitoQ was found to be 24% more effective than CoQ10 at reducing hydrogen peroxide levels in the mitochondria during states of stress. Unlike CoQ10, MitoQ supplementation also increased levels of the important internal antioxidant, catalase, by 36%.

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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

Broome et al. REDOX Biology

DOI: DOI: 10.1016/j.redox.2022.102341 Source

Regular high-intensity exercise leads to adaptations in our bodies and mitochondria that help improve performance and recovery. This study showed that in untrained middle-aged men, just 10 days of supplementation of 20mg/day MitoQ improved exercise performance in middle-aged men (35-55 years old). MitoQ significantly increased peak power generation during a 20km cycling trial compared to placebo. This result was accompanied by an increase in skeletal muscle PGC1α mRNA expression, a gene activator associated with the regulation of mitochondrial health and function.

Read the study

More studies

*Intended for a researcher audience, for research purposes only


HIF-1α promotes cellular growth in lymphatic endothelial cells exposed to chronically elevated pulmonary lymph flow. Boehme JT et al. Scientific Reports. 2016DOI: 10.1038/s41598-020-80882-1 Source

Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels. Méndez D et al. International Journal of Molecular Sciences. 2021DOI: 10.3390/ijms21176192 Source

Effect of treadmill exercise and MitoQ treatment on vascular function in D-galactose-induced senescent mice. Kim DW. 2020DOI: 10.24985/kjss.2019.30.4.689 Source

Mitoquinone attenuates vascular calcification by suppressing oxidative stress and reducing apoptosis of vascular smooth muscle cells via the Keap1/Nrf2 pathway. Cui, L et al. Free Radical Biology and Medicine. 2020DOI: 10.1016/j.freeradbiomed.2020.09.028 Source

Doxorubicin-Induced Oxidative Stress and Endothelial Dysfunction in Conduit Arteries Is Prevented by Mitochondrial-Specific Antioxidant Treatment. Clayton ZS et al. JACC. CardioOncology. 2021DOI: 10.1016/j.jaccao.2020.06.010 Source

Mitochondrial reactive oxygen species scavenging attenuates thrombus formation in a murine model of sickle cell disease. Annarapu GK et al. Journal of thrombosis and haemostasis: JTH. 2022DOI: 10.1111/jth.15298 Source

Reactive Oxygen Species are Essential for Placental Angiogenesis During Early Gestation. Yang Y et al. Oxidative medicine and cellular longevity. 2014DOI: 10.1155/2022/4290922 Source

Mitoquinone ameliorates cigarette smoke-induced airway inflammation and mucus hypersecretion in mice. Yang D et al. International Immunopharmacology. 2021DOI: 10.1016/j.intimp.2020.107149 Source

Autophagy-mitophagy induction attenuates cardiovascular inflammation in a murine model of Kawasaki disease vasculitis. Marek-Iannucci S et al. JCI Insight. 2021DOI: 10.1172/jci.insight.151981 Source

MicroRNA-210-mediated mtROS confer hypoxia-induced suppression of STOCs in ovine uterine arteries. Hu XQ et al. British Journal of Pharmacology. 2022DOI: 10.1111/bph.15914 Source

Mitochondrial-targeted antioxidant supplementation for improving age-related vascular dysfunction in humans: A study protocol. Murray K.O. et al. Frontiers in Physiology. 2022DOI: 10.3389/fphys.2022.980783 Source

Acute mitochondrial antioxidant intake improves endothelial function, antioxidant enzyme activity, and exercise tolerance in patients with peripheral artery disease. Park SY et al. American Journal of Physiology. Heart and Circulatory Physiology. 2020DOI: 10.1152/ajpheart.00235.2020 Source

Effect of Combined Endurance Training and MitoQ on Cardiac Function and Serum Level of Antioxidants, NO, miR-126, and miR-27a in Hypertensive Individuals. Masoumi-Ardakani et al. BioMed Research International. 2022DOI: 10.1155/2022/8720661 Source

Vasodilatory and vascular mitochondrial respiratory function with advancing age: Evidence of a free radically-mediated link in the human vasculature. Park SH et al. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 2020DOI: 10.1152/ajpregu.00268.2019 Source

Chronic supplementation with a mitochondrial antioxidant (MitoQ) improves vascular function in healthy older adults. Rossman MJ et al. Hypertension (Dallas, Tex.: 1979). 2018DOI: 10.1161/HYPERTENSIONAHA.117.10787 Source

Reactive oxygen species induced Ca2+ influx via TRPV4 and microvascular endothelial dysfunction in the SU5416/hypoxia model of pulmonary arterial hypertension. Suresh K et al. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2020DOI: 10.1152/ajplung.00430.2017 Source

Age-related endothelial dysfunction in human skeletal muscle feed arteries: the role of free radicals derived from mitochondria in the vasculature. Park S Y et al. Acta Physiologica (Oxford, England). 2018DOI: 10.1111/apha.12893 Source

Mitochondria-targeted antioxidant therapy with MitoQ ameliorates aortic stiffening in old mice. Gioscia-Ryan RA et al. Journal of Applied Physiology (Bethesda, Md.: 1985). 2018DOI: 10.1152/japplphysiol.00670.2017 Source

Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice. Gioscia-Ryan RA et al. Aging (Albany NY). 2019DOI: 10.18632/aging.101099 Source

Mitochondria-targeted antioxidant MitoQ intercepts superoxide radical formation under acute hypoxia: Evaluation of the oxidative stress in murine pulmonary arterial smooth muscle cells by electron paramagnetic resonance spectroscopy. Scheibe S et al. Free Radical Biology and Medicine. 2018DOI: 10.1016/j.freeradbiomed.2016.04.106 Source

Transgenic overexpression of uncoupling protein 2 attenuates salt-induced vascular dysfunction by inhibition of oxidative stress. Ma S et al. American Journal of Hypertension. 2016DOI: 10.1093/ajh/hpt225 Source

Redox signaling via oxidative inactivation of PTEN modulates pressure-dependent myogenic tone in rat middle cerebral arteries. Gebremedhin D et al. PLoS One. 2012DOI: 10.1371/journal.pone.0068498 Source

Mitochondrial reactive oxygen species enhance AMP-activated protein kinase activation in the endothelium of patients with coronary artery disease and diabetes. Mackenzie RM et al. Clinical Science. 2014DOI: 10.1042/CS20120239 Source

Evidence for a relationship between mitochondrial Complex I activity and mitochondrial aldehyde dehydrogenase during nitroglycerin tolerance: Effects of mitochondrial antioxidants. Garcia-Bou R et al. Biochim Biophys Acta (BBA)-Bioenergetics. 2013DOI: 10.1016/j.bbabio.2012.02.013 Source

Complex I dysfunction and tolerance to nitroglycerin: an approach based on mitochondrial-targeted antioxidants. Esplugues JV et al. Circulation Resarch. 2012DOI: 10.1161/01.RES.0000250430.62775.99 Source


Prohibitin-1 Is a Dynamically Regulated Blood Protein With Cardioprotective Effects in Sepsis. Mattox TA et al. Journal of the American Heart Association. 2021DOI: 10.1161/JAHA.120.019877 Source

Ceramide modulates electrophysiological characteristics and oxidative stress of pulmonary vein cardiomyocytes. Huang SY et al. European Journal of Clinical Investigation. 2022DOI: 10.1111/eci.13690 Source

[Inhibition of mitochondrial reactive oxygen species reduces high glucose-induced pyroptosis and ferroptosis in H9C2 cardiac myocytes]. Wang J et al. Nan Fang Yi Ke Da Xue Xue Bao = Journal of Southern Medical University. 2021DOI: 10.12122/j.issn.1673-4254.2021.07.03 Source

mTOR contributes to endothelium-dependent vasorelaxation by promoting eNOS expression and preventing eNOS uncoupling. Wang Y et al. Communications Biology. 2022DOI: 10.1038/s42003-022-03653-w Source

Endurance training and MitoQ supplementation increases PERM1 and SMYD1 gene expression and improves hemodynamic parameters in cardiac muscle of male Wistar rats. Mahboube ST et al. 2022DOI: 10.21203/ Source

Mitochondrial targeted antioxidants, mitoquinone and SKQ1, not vitamin C, mitigate doxorubicin-induced damage in H9c2 myoblast: pretreatment vs. co-treatment. Sacks B et al. BMC Pharmacology and Toxicology. 2021DOI: 10.1186/s40360-021-00518-6 Source

MicroRNA-210 Controls Mitochondrial Metabolism and Protects Heart Function in Myocardial Infarction. Song R et al. Circulation. 2022DOI: 10.1161/CIRCULATIONAHA.121.056929 Source

Mitochondrial Oxidative Stress Induces Cardiac Fibrosis in Obese Rats through Modulation of Transthyretin. Martínez-Martínez E et al. International Journal of Molecular Sciences. 2022DOI: 10.3390/ijms23158080 Source

The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats - PubMed. Jiménez-González S et al. 2020DOI: 10.3390/cells9020451. Source

The Interplay of Mitochondrial Oxidative Stress and Endoplasmic Reticulum Stress in Cardiovascular Fibrosis in Obese Rats. Souza-Neto FV et al. Antioxidants (Basel, Switzerland). 2021DOI: 10.3390/antiox10081274 Source

Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress. Souza-Neto FV et al. Antioxidants (Basel, Switzerland). 2022DOI: 10.3390/antiox11071232 Source

Effect of mitochondrial-targeted antioxidants on glycaemic control, cardiovascular health, and oxidative stress in humans: A systematic review and meta-analysis of randomized controlled trials. Mason SA et al. Diabetes, Obesity & Metabolism. 2022DOI: 10.1111/dom.14669 Source

Endurance training and MitoQ supplementation improve spatial memory, VEGF expression, and neurogenic factors in hippocampal tissue of rats. Zadeh HJ et al. Journal of Clinical and Translational Research. 2023DOI: 10.18053/jctres.09.202301.001 Source

Chronic mitochondria antioxidant treatment in older adults alters the circulating milieu to improve endothelial cell function and mitochondrial oxidative stress. Murray KO et al. American Journal of Physiology-Heart and Circulatory Physiology. 2023DOI: 10.1152/ajpheart.00270.2023 Source

Cyclovirobuxine D protects against diabetic cardiomyopathy by activating Nrf2-mediated antioxidant responses. Jiang Z et al. Scientific Reports. 2020DOI: 10.1038/s41598-020-63498-3 Source

Regulation of mitochondrial fragmentation in microvascular endothelial cells isolated from the SU5416/hypoxia model of pulmonary arterial hypertension. Suresh K et al. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2019DOI: 10.1152/ajplung.00396.2018 Source

Mitoquinone ameliorates pressure overload-induced cardiac fibrosis and left ventricular dysfunction in mice. Goh KY et al. Redox Biology. 2019DOI: 10.1016/j.redox.2019.101100 Source

G protein-coupled estrogen receptor (GPER) deficiency induces cardiac remodeling through oxidative stress. Wang H et al. Translational Research. 2018DOI: 10.1016/j.trsl.2018.04.005 Source

Ice-free cryopreservation of heart valve tissue: The effect of adding MitoQ to a VS83 formulation and its influence on mitochondrial dynamics. Sui Y et al. Cryobiology. 2018DOI: 10.1016/j.cryobiol.2018.01.008 Source

P 165 - The role of mitochondrial reactive oxygen species in the response of the pulmonary vasculature to hypoxia and right heart remodeling. Scheibe S et al. Free Radical Biology and Medicine. 2017DOI: 10.1016/j.freeradbiomed.2017.04.250 Source

Differences in the profile of protection afforded by TRO40303 and mild hypothermia in models of cardiac ischemia/reperfusion injury. Hannson MJ et al. European Journal of Pharmacology. 2015DOI: 10.1016/j.ejphar.2015.04.009 Source

Cardiomyocyte mitochondrial oxidative stress and cytoskeletal breakdown in the heart with a primary volume overload. Yancey DM et al. American Journal of Physiology-Heart and Circulatory Physiology. 2015DOI: 10.1152/ajpheart.00638.2014 Source

Mitochondria transmit apoptosis signalling in cardiomyocyte-like cells and isolated hearts exposed to experimental ischemia-reperfusion injury. Neuzil J et al. Redox Report: Communications in Free Radical Research. 2007DOI: 10.1179/135100007X200227 Source

Slow calcium waves and redox changes precede mitochondrial permeability transition pore opening in the intact heart during hypoxia and reoxygenation. Davidson SM et al. Cardiovascular Research. 2012DOI: 10.1093/cvr/cvr349 Source

Resolution of Mitochondrial Oxidative Stress Rescues Coronary Collateral Growth in Zucker Obese Fatty Rats. Fen Pung Y et al. Arteriosclerosis, Thrombosis and Vascular Biology. 2012DOI: 10.1161/ATVBAHA.111.241802 Source

Novel insights into interactions between mitochondria and xanthine oxidase in acute cardiac volume overload. Gladden JD et al. Free Radical Biology and Medicine. 2011DOI: 10.1016/j.freeradbiomed.2011.08.022 Source

Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury. Adlam VJ et al. FASEB journal: official publication of the Federation of American Societies for Experimental Biology. 2005DOI: 10.1096/fj.05-3718com Source


Generation of mitochondrial reactive oxygen species is controlled by ATPase inhibitory factor 1 and regulates cognition. Esparza-Moltó PB et al. PLoS biology. 2021DOI: 10.1371/journal.pbio.3001252 Source

Preeclamptic placentae release factors that damage neurons: implications for foetal programming of disease. Scott H et al. Neuronal Signaling. 2018DOI: 10.1042/NS20180139 Source

The Role of Pink1-Mediated Mitochondrial Pathway in Propofol-Induced Developmental Neurotoxicity. Liang C et al. Neurochemical Research. 2021DOI: 10.1007/s11064-021-03359-1 Source

Accelerated aging of the brain transcriptome by the common chemotherapeutic doxorubicin. Cavalier AN et al. Experimental Gerontology. 2021DOI: 10.1016/j.exger.2021.111451 Source

Mitochondrial Reactive Oxygen Species Mediate Activation of TRPV1 and Calcium Entry Following Peripheral Sensory Axotomy - PubMed. Kievit B. 2022DOI: 10.3389/fnmol.2022.852181 Source

Recent Advances in Molecular Pathways and Therapeutic Implications Targeting Mitochondrial Dysfunction for Alzheimer's Disease. Dhapola R et al. Molecular Neurobiology. 2022DOI: 10.1007/s12035-021-02612-6 Source

Mitigation of CNS oxygen toxicity seizures: evaluating the neuroprotective effects of L-NAME versus Mitoquinone during exposure to 5 ATA O2 in freely behaving Sprague-Dawley rats. Hinojo CM et al. The FASEB Journal. 2022DOI: 10.1096/fasebj.2022.36.S1.R4180 Source

Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex. Olajide OJ et al. Frontiers in Aging Neuroscience. 2022DOI: 10.3389/fnagi.2022.960314 Source

Long-term mitochondrial stress induces early steps of Tau aggregation by increasing reactive oxygen species levels and affecting cellular proteostasis. Samluk L et al. Molecular Biology of the Cell. 2022DOI: 10.1091/mbc.E21-11-0553 Source

Perturbed actin cap as a new personalized biomarker in primary fibroblasts of Huntington's disease patients. Gharaba S et al. Frontiers in Cell and Developmental Biology. 2023DOI: 10.3389/fcell.2023.1013721 Source

Apolipoprotein E Polymorphism Impacts White Matter Injury Through Microglial Phagocytosis After Experimental Subarachnoid Hemorrhage. Li C et al. Neuroscience. 2023DOI: 10.1016/j.neuroscience.2023.05.020 Source

Quinones as Neuroprotective Agents. Cores Á et al. Antioxidants. 2023DOI: 10.3390/antiox12071464 Source

A mitochondrial-targeted antioxidant (MitoQ) improves motor coordination and reduces Purkinje cell death in a mouse model of ARSACS. Márquez BT et al. Neurobiology of Disease. 2023DOI: 10.1016/j.nbd.2023.106157 Source

CREB Protects against Temporal Lobe Epilepsy Associated with Cognitive Impairment by Controlling Oxidative Neuronal Damage. Xing et al. Neurodegenerative Diseases. 2020DOI: 10.1159/000507023 Source

Neuroprotective Benefits of Exercise and MitoQ on Memory Function, Mitochondrial Dynamics, Oxidative Stress, and Neuroinflammation in D-Galactose-Induced Aging Rats. Jeong et al. Brain Sciences. 2021DOI: 10.3390/brainsci11020164 Source

Mitochondria: Novel Mechanisms and Therapeutic Targets for Secondary Brain Injury After Intracerebral Hemorrhage. Chen et al. Frontiers in Aging Neuroscience. 2021DOI: 10.3389/fnagi.2020.615451 Source

Treating Neurodegenerative Disease with Antioxidants: Efficacy of the Bioactive Phenol Resveratrol and Mitochondrial-Targeted MitoQ and SkQ. Shinn et al. Antioxidants. 2021DOI: 10.3390/antiox10040573 Source

Effective therapeutic strategies in a preclinical mouse model of Charcot–Marie–Tooth disease. Nuevo-Tapioles et al. Human Molecular Genetics. 2021DOI: 10.1093/hmg/ddab207 Source

Mitochondrial, exosomal miR137-COX6A2 and gamma synchrony as biomarkers of parvalbumin interneurons, psychopathology, and neurocognition in schizophrenia. Khadimallah et al. Molecular Psychiatry. 2022DOI: 10.1038/s41380-021-01313-9 Source

Mitoquinone supplementation alleviates oxidative stress and pathologic outcomes following repetitive mild TBI at a chronic time point. Tabet et al. Experimental Neurology. 2022DOI: 10.1016/j.expneurol.2022.113987 Source

The peroxisomal fatty acid transporter ABCD1/PMP-4 is required in the C. elegans hypodermis for axonal maintenance: A worm model for adrenoleukodystrophy. Coppa A et al. Free Radical Biology and Medicine. 2020DOI: 10.1016/j.freeradbiomed.2020.01.177 Source

Mitoquinone alleviates vincristine-induced neuropathic pain through inhibiting oxidative stress and apoptosis via the improvement of mitochondrial dysfunction. Chen X et al. Biomedicine & Pharmacotherapy. 2020DOI: 10.1016/j.biopha.2020.110003 Source

Involvement of oxidative stress and mitochondrial mechanisms in air pollution-related neurobiological impairments. Salvi A et al. Neurobiology of Stress. 2020DOI: 10.1016/j.ynstr.2019.100205 Source

Role of the mitochondrial calcium uniporter in Mg2+-free-induced epileptic hippocampal neuronal apoptosis. Li Y et al. International Journal od Neuroscience. 2020DOI: 10.1080/00207454.2020.1715978 Source

Neuroprotective effects of mitoquinone and oleandrin on Parkinson’s disease model in zebrafish. Ünal I et al. International Journal of Neuroscience. 2020DOI: 10.1080/00207454.2019.1698567 Source

The interplay between redox signalling and proteostasis in neurodegeneration: In vivo effects of a mitochondria-targeted antioxidant in Huntington's disease mice. Pinho BR et al. Free Radical Biology and Medicine. 2020DOI: 10.1016/j.freeradbiomed.2019.11.021 Source

Mitophagy reduces oxidative stress via Keap1/Nrf2/PHB2 pathway after SAH in rats. Zhang T et al. Stroke. 2019DOI: 10.1161/STROKEAHA.118.021590 Source

Mitoquinone attenuates blood-brain barrier disruption through Nrf2/PHB2/OPA1 pathway after subarachnoid hemorrhage in rats. Zhang et al. Experimental Neurology. 2019DOI: 10.1016/j.expneurol.2019.02.009 Source

Therapeutic potential of the mitochondria-targeted antioxidant MitoQ in mitochondrial-ROS induced sensorineural hearing loss caused by Idh2 deficiency. Kim YR et al. Redox Biology. 2019DOI: 10.1016/j.redox.2018.11.013 Source

Effects of NADPH Oxidase Inhibitors and Mitochondria-Targeted Antioxidants on Amyloid β1-42-Induced Neuronal Deaths in Mouse Mixed Cortical Cultures. Hwang S et al. Chonnam Medical Journal. 2018DOI: 10.4068/cmj.2018.54.3.159 Source

Mitochondrial-targeted antioxidant MitoQ provides neuroprotection and reduces neuronal apoptosis in experimental traumatic brain injury possibly via the Nrf2-ARE pathway. Zhou J et al. American Journal of Translational Research. 2018;10(6):1887-1899. eCollection 2018Source

Neuronal Dysfunction Associated with Cholesterol Deregulation. Marcuzzi A et al. International Journal of Molecular Sciences. 2018DOI: 10.3390/ijms19051523 Source

Mitigating peroxynitrite mediated mitochondrial dysfunction in aged rat brain by mitochondria-targeted antioxidant MitoQ. Maiti AK et al. Biogerontology. 2018DOI: 10.1007/s10522-018-9756-6 Source

Mitochondrial rescue prevents glutathione peroxidase-dependent ferroptosis. Jelinek A et al. Free Radical Biology and Medicine. 2018DOI: 10.1016/j.freeradbiomed.2018.01.019 Source

Selective Mitochondrial Targeting Exerts Anxiolytic Effects In Vivo. Nussbaumer M et al. Neuropsychopharmacology. 2016DOI: 10.1038/npp.2015.341 Source

Mitochondrial redox and pH signaling occurs in axonal and synaptic organelle clusters. Breckwoldt MO et al. Scientific Reports. 2016DOI: 10.1038/srep23251 Source

Mitochondria-derived reactive oxygen species mediate caspase-dependent and -independent neuronal deaths. Manus MJ et al. Mol Cell Neurosci. 2014DOI: 10.1016/j.mcn.2014.09.002 Source

The LRRK2 inhibitor GSK2578215A induces protective autophagy in SH-SY5Y cells: involvement of Drp-1-mediated mitochondrial fission and mitochondrial-derived ROS signaling. Saez-Atienzar S et al. Cell Death & Disease. 2014DOI: 10.1038/cddis.2014.320 Source

Neurological deficits caused by tissue hypoxia in neuroinflammatory disease. Davies Al et al. Annals of Neurology. 2013DOI: 10.1002/ana.24006 Source

Glucagon-Like Peptide-1 Cleavage Product GLP-1(9-36) Amide Rescues Synaptic Plasticity and Memory Deficits in Alzheimer's Disease Model Mice. Ma T et al. The Journal of Neuroscience. 2012DOI: 10.1523/JNEUROSCI.2107-12.2012 Source

Amyloid β-Induced Impairments in Hippocampal Synaptic Plasticity Are Rescued by Decreasing Mitochondrial Superoxide. Ma T et al. The Journal of Neuroscience. 2011DOI: 10.1523/JNEUROSCI.6566-10.2011 Source

Neuroprotection by a mitochondria-targeted drug in a Parkinson's disease model. Ghosh A et al. Free Radical Biology and Medicine. 2010DOI: 10.1016/j.freeradbiomed.2010.08.028 Source

Mitochondria-Targeted Antioxidants Protect Against Amyloid-β Toxicity in Alzheimer's Disease Neurons. Manczak M et al. Journal of Alzheimer’s Disease. 2010DOI: 10.3233/JAD-2010-100564 Source

Mitochondrial Dysfunction in SOD1G93A-Bearing Astrocytes Promotes Motor Neuron Degeneration: Prevention by Mitochondrial-Targeted Antioxidants. Cassina P et al. The Journal of Neuroscience. 2008DOI: 10.1523/JNEUROSCI.5308-07.2008 Source

Mitochondrial Superoxide Production and Nuclear Factor Erythroid 2-Related Factor 2 Activation in p75 Neurotrophin Receptor-Induced Motor Neuron Apoptosis. Pehar M et al. The Journal of Neuroscience. 2007DOI: 10.1523/JNEUROSCI.0823-07.2007 Source

Manganese potentiates lipopolysaccharide-induced expression of NOS2 in C6 glioma cells through mitochondrial-dependent activation of nuclear factor kappaB. Barhoumi R et al. Molecular Brain Research. 2004DOI: 10.1016/j.molbrainres.2003.12.009 Source


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