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Mitoq

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https://www.readbyqxmd.com/read/29452078/ice-free-cryopreservation-of-heart-valve-tissue-the-effect-of-adding-mitoq-to-a-vs83-formulation-and-its-influence-on-mitochondrial-dynamics
#1
Yulong Sui, Qing Fan, Bin Wang, Jixian Wang, Qing Chang
No abstract text is available yet for this article.
February 13, 2018: Cryobiology
https://www.readbyqxmd.com/read/29421236/mitoq-improves-mitochondrial-dysfunction-in-heart-failure-induced-by-pressure-overload
#2
Rogério Faustino Ribeiro Junior, Erinne Rose Dabkowski, Kadambari Chandra Shekar, Kelly A O Connell, Peter A Hecker, Michael P Murphy
Heart failure remains a major public-health problem with an increase in the number of patients worsening from this disease. Despite current medical therapy, the condition still has a poor prognosis. Heart failure is complex but mitochondrial dysfunction seems to be an important target to improve cardiac function directly. Our goal was to analyze the effects of MitoQ (100 µM in drinking water) on the development and progression of heart failure induced by pressure overload after 14 weeks. The main findings are that pressure overload-induced heart failure in rats decreased cardiac function in vivo that was not altered by MitoQ...
February 1, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29419444/impact-of-the-mitochondria-targeted-antioxidant-mitoq-on-hypoxia-induced-pulmonary-hypertension
#3
Oleg Pak, Susan Scheibe, Azadeh Esfandiary, Mareike Gierhardt, Akylbek Sydykov, Angela Logan, Athanasios Fysikopoulos, Florian Veit, Matthias Hecker, Florian Kroschel, Karin Quanz, Alexandra Erb, Katharina Schäfer, Mirja Fassbinder, Nasim Alebrahimdehkordi, Hossein A Ghofrani, Ralph T Schermuly, Ralf P Brandes, Werner Seeger, Michael P Murphy, Norbert Weissmann, Natascha Sommer
Increased mitochondrial reactive oxygen species (ROS), particularly superoxide have been suggested to mediate hypoxic pulmonary vasoconstriction (HPV), chronic hypoxia-induced pulmonary hypertension (PH) and right ventricular (RV) remodelling.We determined ROS in acute, chronic hypoxia and investigated the effect of the mitochondria-targeted antioxidant MitoQ under these conditions.The effect of MitoQ or its inactive carrier substance, decyltriphenylphosphonium (TPP+), on acute HPV (1% O2 for 10 minutes) was investigated in isolated blood-free perfused mouse lungs...
February 1, 2018: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/29388466/reactive-oxygen-species-induced-ca2-influx-via-trpv4-and-microvascular-endothelial-dysfunction-in-the-su5416-hypoxia-model-of-pulmonary-arterial-hypertension
#4
Karthik Suresh, Laura Servinsky, Haiyang Jiang, Zahna Bigham, Xin Yun, Corinne Kliment, John C Huetsch, Mahendra Damarla, Larissa A Shimoda
Pulmonary arterial hypertension (PAH) is a lethal disease characterized by elevations in pulmonary arterial pressure, in part due to formation of occlusive lesions in the distal arterioles of the lung. These complex lesions may comprise multiple cell types, including endothelial cells (ECs). To better understand the molecular mechanisms underlying EC dysfunction in PAH, lung microvascular endothelial cells (MVECs) were isolated from normoxic rats (N-MVEC) and rats subjected to SU5416 plus hypoxia (SuHx), an experimental model of PAH...
February 1, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29378335/mitochondrial-rescue-prevents-glutathione-peroxidase-dependent-ferroptosis
#5
Anja Jelinek, Lukas Heyder, Michael Daude, Matthias Plessner, Sylvia Krippner, Robert Grosse, Wibke E Diederich, Carsten Culmsee
Research into oxidative cell death is producing exciting new mechanisms, such as ferroptosis, in the neuropathologies of cerebral ischemia and hemorrhagic brain insults. Ferroptosis is an oxidative form of regulated necrotic cell death featuring glutathione (GSH) depletion, disrupted glutathione peroxidase-4 (GPX4) redox defense and detrimental lipid reactive oxygen species (ROS) formation. Further, our recent findings identified mitochondrial damage in models of oxidative glutamate toxicity, glutathione peroxidase depletion, and ferroptosis...
January 26, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29317239/protective-effect-of-mitochondrial-targeted-antioxidant-mitoq-against-iron-ion-56fe-radiation-induced-brain-injury-in-mice
#6
Lu Gan, Zhenhua Wang, Jing Si, Rong Zhou, Chao Sun, Yang Liu, Yancheng Ye, Yanshan Zhang, Zhiyuan Liu, Hong Zhang
Exposure to iron ion 56Fe radiation (IR) during space missions poses a significant risk to the central nervous system and radiation exposure is intimately linked to the production of reactive oxygen species (ROS). MitoQ is a mitochondria-targeted antioxidant that has been shown to decrease oxidative damage and lower mitochondrial ROS in a number of animal models. Therefore, the present study aimed to investigate role of the mitochondrial targeted antioxidant MitoQ against 56Fe particle irradiation-induced oxidative damage and mitochondria dysfunction in the mouse brains...
January 6, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29289511/opening-of-voltage-dependent-anion-channels-promotes-reactive-oxygen-species-generation-mitochondrial-dysfunction-and-cell-death-in-cancer-cells
#7
David N DeHart, Diana Fang, Kareem Heslop, Li Li, John J Lemasters, Eduardo N Maldonado
Enhancement of aerobic glycolysis and suppression of mitochondrial metabolism characterize the pro-proliferative Warburg phenotype of cancer cells. High free tubulin in cancer cells closes voltage dependent anion channels (VDAC) to decrease mitochondrial membrane potential (ΔΨ), an effect antagonized by erastin, the canonical promotor of ferroptosis. Previously, we identified six compounds (X1-X6) that also block tubulin-dependent mitochondrial depolarization. Here, we hypothesized that VDAC opening after erastin and X1-X6 increases mitochondrial metabolism and reactive oxygen species (ROS) formation, leading to ROS-dependent mitochondrial dysfunction, bioenergetic failure and cell death...
December 28, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29194212/evaluation-of-mitoquinone-for-protecting-against-amikacin-induced-ototoxicity-in-guinea-pigs
#8
Carolyn O Dirain, Maria Raye Ann V Ng, Bailey Milne-Davies, Jerin K Joseph, Patrick J Antonelli
HYPOTHESIS: Mitoquinone (MitoQ) attenuates amikacin ototoxicity in guinea pigs. BACKGROUND: MitoQ, a mitochondria-targeted derivative of the antioxidant ubiquinone, has improved bioavailability and demonstrated safety in humans. Thus, MitoQ is a promising therapeutic approach for protecting against amikacin-induced ototoxicity. METHODS: Both oral and subcutaneous administrations of MitoQ were tested. Amikacin-treated guinea pigs (n = 12-18 per group) received water alone (control) or MitoQ 30 mg/l-supplemented drinking water; or injected subcutaneously with 3 to 5 mg/kg MitoQ or saline (control)...
November 29, 2017: Otology & Neurotology
https://www.readbyqxmd.com/read/29156373/mitochondria-targeted-ubiquinone-mitoq-enhances-acetaldehyde-clearance-by-reversing-alcohol-induced-posttranslational-modification-of-aldehyde-dehydrogenase-2-a-molecular-mechanism-of-protection-against-alcoholic-liver-disease
#9
Liuyi Hao, Qian Sun, Wei Zhong, Wenliang Zhang, Xinguo Sun, Zhanxiang Zhou
Alcohol metabolism in the liver generates highly toxic acetaldehyde. Breakdown of acetaldehyde by aldehyde dehydrogenase 2 (ALDH2) in the mitochondria consumes NAD(+) and generates reactive oxygen/nitrogen species, which represents a fundamental mechanism in the pathogenesis of alcoholic liver disease (ALD). A mitochondria-targeted lipophilic ubiquinone (MitoQ) has been shown to confer greater protection against oxidative damage in the mitochondria compared to untargeted antioxidants. The present study aimed to investigate if MitoQ could preserve mitochondrial ALDH2 activity and speed up acetaldehyde clearance, thereby protects against ALD...
November 11, 2017: Redox Biology
https://www.readbyqxmd.com/read/29123192/targeted-mitochondrial-therapy-using-mitoq-shows-equivalent-renoprotection-to-angiotensin-converting-enzyme-inhibition-but-no-combined-synergy-in-diabetes
#10
Micheal S Ward, Nicole B Flemming, Linda A Gallo, Amelia K Fotheringham, Domenica A McCarthy, Aowen Zhuang, Peter H Tang, Danielle J Borg, Hannah Shaw, Benjamin Harvie, David R Briskey, Llion A Roberts, Manuel R Plan, Michael P Murphy, Mark P Hodson, Josephine M Forbes
Mitochondrial dysfunction is a pathological mediator of diabetic kidney disease (DKD). Our objective was to test the mitochondrially targeted agent, MitoQ, alone and in combination with first line therapy for DKD. Intervention therapies (i) vehicle (D); (ii) MitoQ (DMitoQ;0.6 mg/kg/day); (iii) Ramipril (DRam;3 mg/kg/day) or (iv) combination (DCoAd) were administered to male diabetic db/db mice for 12 weeks (n = 11-13/group). Non-diabetic (C) db/m mice were followed concurrently. No therapy altered glycaemic control or body weight...
November 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29074712/mitochondria-targeted-antioxidant-therapy-with-mitoq-ameliorates-aortic-stiffening-in-old-mice
#11
Rachel A Gioscia-Ryan, Micah L Battson, Lauren M Cuevas, Jason S Eng, Michael P Murphy, Douglas R Seals
Aortic stiffening is a major independent risk factor for cardiovascular diseases, cognitive dysfunction and other chronic disorders of aging. Mitochondria-derived reactive oxygen species are a key source of arterial oxidative stress which may contribute to arterial stiffening by promoting adverse structural changes-including collagen overabundance and elastin degradation-and enhancing inflammation, but the potential for mitochondria-targeted therapeutic strategies to ameliorate aortic stiffening with primary aging is unknown...
October 26, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/29070589/mitochondria-targeted-molecules-determine-the-redness-of-the-zebra-finch-bill
#12
Alejandro Cantarero, Carlos Alonso-Alvarez
The evolution and production mechanisms of red carotenoid-based ornaments in animals are poorly understood. Recently, it has been suggested that enzymes transforming yellow carotenoids to red pigments (ketolases) in animal cells may be positioned in the inner mitochondrial membrane (IMM) intimately linked to the electron transport chain. These enzymes may mostly synthesize coenzyme Q10 (coQ10), a key redox-cycler antioxidant molecularly similar to yellow carotenoids. It has been hypothesized that this shared pathway favours the evolution of red traits as sexually selected individual quality indices by revealing a well-adjusted oxidative metabolism...
October 2017: Biology Letters
https://www.readbyqxmd.com/read/28993480/mitochondrial-abnormality-facilitates-cyst-formation-in-autosomal-dominant-polycystic-kidney-disease
#13
Yu Ishimoto, Reiko Inagi, Daisuke Yoshihara, Masanori Kugita, Shizuko Nagao, Akira Shimizu, Norihiko Takeda, Masaki Wake, Kenjiro Honda, Jing Zhou, Masaomi Nangaku
Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most common inherited kidney disease. Mutations in the PKD1 and PKD2 genes, encoding respective polycystin-1 and polycystin-2 Ca2+ ion channels, results in tubular epithelial cell-derived renal cysts. Recent clinical studies demonstrate oxidative stress as present early in ADPKD. Mitochondria comprise the primary reactive oxygen species source and also their main effector target; however, the pathophysiological role of mitochondria in ADPKD remains uncharacterized...
October 9, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28898446/contradictory-effects-of-mitochondria-and-non-mitochondria-targeted-antioxidants-on-hepatocarcinogenesis-by-altering-dna-repair
#14
Bibo Wang, Jing Fu, Ting Yu, An Xu, Wenhao Qin, Zhishi Yang, Yao Chen, Hongyang Wang
Conflicting effects of antioxidant supplementation on cancer prevention or promotion is of great concern to healthy people and cancer patients. Despite recent studies about antioxidants accelerating the progression of lung cancer and melanoma, it does not fully deny antioxidants for cancer prevention. Both tumor and antioxidants types influence the actual efficacy. However, little is known about the impact of different types of antioxidants on primary hepatocellular carcinoma (HCC), including non-mitochondrial- and mitochondrial-targeted antioxidants...
September 12, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28831049/treating-the-placenta-to-prevent-adverse-effects-of-gestational-hypoxia-on-fetal-brain-development
#15
Tom J Phillips, Hannah Scott, David A Menassa, Ashleigh L Bignell, Aman Sood, Jude S Morton, Takami Akagi, Koki Azuma, Mark F Rogers, Catherine E Gilmore, Gareth J Inman, Simon Grant, Yealin Chung, Mais M Aljunaidy, Christy-Lynn Cooke, Bruno R Steinkraus, Andrew Pocklington, Angela Logan, Gavin P Collett, Helena Kemp, Peter A Holmans, Michael P Murphy, Tudor A Fulga, Andrew M Coney, Mitsuru Akashi, Sandra T Davidge, C Patrick Case
Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes...
August 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28774709/treatment-with-antioxidants-ameliorates-oxidative-damage-in-a-mouse-model-of-propionic-acidemia
#16
Ana Rivera-Barahona, Esmeralda Alonso-Barroso, Belén Pérez, Michael P Murphy, Eva Richard, Lourdes R Desviat
Oxidative stress contributes to the pathogenesis of propionic acidemia (PA), a life threatening disease caused by the deficiency of propionyl CoA-carboxylase, in the catabolic pathway of branched-chain amino acids, odd-number chain fatty acids and cholesterol. Patients develop multisystemic complications including seizures, extrapyramidal symptoms, basal ganglia deterioration, pancreatitis and cardiomyopathy. The accumulation of toxic metabolites results in mitochondrial dysfunction, increased reactive oxygen species and oxidative damage, all of which have been documented in patients' samples and in a hypomorphic mouse model...
September 2017: Molecular Genetics and Metabolism
https://www.readbyqxmd.com/read/28656516/targeting-mitochondrial-calcium-handling-and-reactive-oxygen-species-in-heart-failure
#17
REVIEW
Alexander Dietl, Christoph Maack
PURPOSE OF REVIEW: In highly prevalent cardiac diseases, new therapeutic approaches are needed. Since the first description of oxidative stress in heart failure, reactive oxygen species (ROS) have been considered as attractive drug targets. Though clinical trials evaluating antioxidant vitamins as ROS-scavenging agents yielded neutral results in patients at cardiovascular risk, the knowledge of ROS as pathophysiological factors has considerably advanced in the past few years and led to novel treatment approaches...
August 2017: Current Heart Failure Reports
https://www.readbyqxmd.com/read/28608403/mitochondria-targeted-antioxidant-mitoq-reduced-renal-damage-caused-by-ischemia-reperfusion-injury-in-rodent-kidneys-longitudinal-observations-of-t2-weighted-imaging-and-dynamic-contrast-enhanced-mri
#18
Xiaoge Liu, Michael P Murphy, Wei Xing, Huanhuan Wu, Rui Zhang, Haoran Sun
PURPOSE: To investigate the effect of mitochondria-targeted antioxidant MitoQ in reducing the severity of renal ischemia-reperfusion injury (IRI) in rats using T2 -weighted imaging and dynamic contrast-enhanced MRI (DCE-MRI). METHODS: Ischemia-reperfusion injury was induced by temporarily clamping the left renal artery. Rats were pretreated with MitoQ or saline. The MRI examination was performed before and after IRI (days 2, 5, 7, and 14). The T2 -weighted standardized signal intensity of the outer stripe of the outer medulla (OSOM) was measured...
June 12, 2017: Magnetic Resonance in Medicine: Official Journal of the Society of Magnetic Resonance in Medicine
https://www.readbyqxmd.com/read/28595656/ros-production-induced-by-braf-inhibitor-treatment-rewires-metabolic-processes-affecting-cell-growth-of-melanoma-cells
#19
Giulia Cesi, Geoffroy Walbrecq, Andreas Zimmer, Stephanie Kreis, Claude Haan
BACKGROUND: Most melanoma patients with BRAF(V600E) positive tumors respond well to a combination of BRAF kinase and MEK inhibitors. However, some patients are intrinsically resistant while the majority of patients eventually develop drug resistance to the treatment. For patients insufficiently responding to BRAF and MEK inhibitors, there is an ongoing need for new treatment targets. Cellular metabolism is such a promising new target line: mutant BRAF(V600E) has been shown to affect the metabolism...
June 8, 2017: Molecular Cancer
https://www.readbyqxmd.com/read/28522560/effect-of-long-term-maternal-smoking-on-the-offspring-s-lung-health
#20
Surpon Sukjamnong, Yik Lung Chan, Razia Zakarya, Sonia Saad, Pawan Sharma, Rachana Santiyanont, Hui Chen, Brian G Oliver
Maternal smoking during pregnancy contributes to long-term health problems in offspring, especially respiratory disorders that can manifest in either childhood or adulthood. Receptors for advanced glycation end products (RAGE) are multiligand receptors abundantly localized in the lung, capable of responding to by-products of reactive oxygen species and proinflammatory responses. RAGE signaling is a key regulator of inflammation in cigarette smoking-related pulmonary diseases. However, the impact of maternal cigarette smoke exposure on lung RAGE signaling in the offspring is unclear...
August 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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