Therapeutic Targeting of Mitochondrial Superoxide in Hypertension
By A. Dikalova, Alfiya Bikineyeva, K. Budzyn, R. Nazarewicz, Louise A. McCann, W. Lewis, David G. Harrison, S. Dikalov. Circulation Research, 2010
724 citations recorded by the source corpus.
Superoxide (O2•) has been implicated in the pathogenesis of many human diseases including hypertension, however commonly employed antioxidants have proven ineffective in clinical trials. It is possible that these agents are not adequately delivered to the subcellular sites of O2• production.
Subfields: Cardiology and Cardiovascular Medicine, Nutrition and Dietetics, Physiology
View Paper: https://www.semanticscholar.org/paper/2ee7c4e98d103fc943a188f30a72fcd5a7121235
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In Cardiology and Cardiovascular Medicine
In Nutrition and Dietetics
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Citations in the corpus
- Crosstalk between mitochondria and NADPH oxidases (2011, methodology): “It is important to note thatmitoTEMPO treatment inhibited cellularO2 andmimickedSOD2overexpression inSOD2-depleted cells, rescuing SOD2-depleted cells [21].”
- Ferroptosis as a target for protection against cardiomyopathy (2019, background): “MitoTEMPO, a superoxide scavenger designed to target the mitochondria, can readily pass through lipid bilayers and accumulates selectively in mitochondria (45).”
- Biological Activities of Reactive Oxygen and Nitrogen Species: Oxidative Stress versus Signal Transduction (2015, background): “However, treatment with mitoTEMPO, a mitochondria-targeted antioxidant, or overexpression of mitochondrial SOD captured O2• and decreased the activation of vascular NADPH oxidases [60].”
- Vascular Inflammation and Oxidative Stress: Major Triggers for Cardiovascular Disease (2019, background): “There are also activation pathways between different ROS sources in a crosstalk fashion [101–103], which was mainly demonstrated for the NOX-2/mitochondrial axis [104, 105], eNOS uncoupling, and xanthine dehydrogenase/oxidase conversion [77, 78], where “ROS-induced ROS formation” can be found as ori”
- Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, background): “The critical role of mitochondrial ROS in such a signaling process that amplifies cellular ROS production in response to either angiotensin II [463] or hypoxia [462] is supported by studies that have employed targeted over-expression or inhibition of either MnSOD or glutathione peroxidase in mitocho”
- Cardiac Metabolism and Its Interactions with Contraction, Growth, and Survival of the Cardiomyocte (2013, background): “MitoTEMPO, a superoxide and alkyl scavenger, demonstrated cardioprotective effects in hypertension and diabetes mellitus models.(175,176) EUK8, a superoxide dismutase and catalase mimetic, rescued cardiac dysfunction in genetic models of increased oxidative stress.”
- Oxidative Stress in Obesity: A Critical Component in Human Diseases (2014, background): “It has also been reported that mitochondria-targeted antioxidants inhibit ROS production by mitochondria, reducing NOX activity [23].”
- Superoxide Dismutases: Role in Redox Signaling, Vascular Function, and Diseases (2011, neutral): “Mitochondria-targeted SOD mimetic mitoTEMPO or overexpression of SOD2 improves endothelial function and reduces hypertension and oxidative stress in mice with Ang II– or DOCA salt-induced hypertension, but not in normotensive mice (52).”
- Mitochondrial function as a therapeutic target in heart failure (2016, neutral): “This approach to therapy, however, might ultimately succeed when novel scavenging compounds that overcome permeability and targeting problems, such as XJB-5-131 (REFS 122,123) , mitoTEMPO 124,125 , and EUK8/EUK134 (REFS 126–128) , are tested in humans.”