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https://www.readbyqxmd.com/read/28993480/mitochondrial-abnormality-facilitates-cyst-formation-in-autosomal-dominant-polycystic-kidney-disease
#1
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 Ca(2+) 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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
https://www.readbyqxmd.com/read/28494869/mitochondrial-ros-production-protects-the-intestine-from-inflammation-through-functional-m2-macrophage-polarization
#9
Laura Formentini, Fulvio Santacatterina, Cristina Núñez de Arenas, Konstantinos Stamatakis, David López-Martínez, Angela Logan, Manuel Fresno, Ron Smits, Michael P Murphy, José M Cuezva
Mitochondria are signaling hubs in cellular physiology that play a role in inflammatory diseases. We found that partial inhibition of the mitochondrial ATP synthase in the intestine of transgenic mice triggers an anti-inflammatory response through NFκB activation mediated by mitochondrial mtROS. This shielding phenotype is revealed when mice are challenged by DSS-induced colitis, which, in control animals, triggers inflammation, recruitment of M1 pro-inflammatory macrophages, and the activation of the pro-oncogenic STAT3 and Akt/mTOR pathways...
May 9, 2017: Cell Reports
https://www.readbyqxmd.com/read/28493603/age-related-endothelial-dysfunction-in-human-skeletal-muscle-feed-arteries-the-role-of-free-radicals-derived-from-mitochondria-in-the-vasculature
#10
Song-Young Park, Oh Sung Kwon, Robert H I Andtbacka, John R Hyngstrom, Van Reese, Michael P Murphy, Russell S Richardson
AIM: This study sought to determine the role of free radicals derived from mitochondria in the vasculature in the recognized age-related endothelial dysfunction of human skeletal muscle feed arteries (SMFAs). METHODS: A total of 44 SMFAs were studied with and without acute exposure to the mitochondria-targeted antioxidant MitoQ and nitric oxide synthase (NOS) blockade. The relative abundance of proteins from the electron transport chain, phosphorylated (p-) to endothelial (e) NOS ratio, manganese superoxide dismutase (MnSOD), and the mitochondria-derived superoxide (O2(-) ) levels were assessed in SMFA...
May 11, 2017: Acta Physiologica
https://www.readbyqxmd.com/read/28463821/mitochondrial-ros-induced-by-chronic-ethanol-exposure-promote-hyper-activation-of-the-nlrp3-inflammasome
#11
Laura R Hoyt, Matthew J Randall, Jennifer L Ather, Daniel P DePuccio, Christopher C Landry, Xi Qian, Yvonne M Janssen-Heininger, Albert van der Vliet, Anne E Dixon, Eyal Amiel, Matthew E Poynter
Alcohol use disorders are common both in the United States and globally, and are associated with a variety of co-morbid, inflammation-linked diseases. The pathogenesis of many of these ailments are driven by the activation of the NLRP3 inflammasome, a multi-protein intracellular pattern recognition receptor complex that facilitates the cleavage and secretion of the pro-inflammatory cytokines IL-1β and IL-18. We hypothesized that protracted exposure of leukocytes to ethanol would amplify inflammasome activation, which would help to implicate mechanisms involved in diseases associated with both alcoholism and aberrant NLRP3 inflammasome activation...
August 2017: Redox Biology
https://www.readbyqxmd.com/read/28357127/metabolic-effects-of-a-mitochondrial-targeted-coenzyme-q-analog-in-high-fat-fed-obese-mice
#12
Brian D Fink, Deng Fu Guo, Chaitanya A Kulkarni, Kamal Rahmouni, Robert J Kerns, William I Sivitz
We recently reported that mitoquinone (mitoQ, 500 μmol/L) added to drinking water of C57BL/6J mice attenuated weight gain, decreased food intake, increased hypothalamic orexigenic gene expression, and mitigated oxidative stress when administered from the onset of high-fat (HF) feeding. Here, we examined the effects of mitoQ on pre-existing obesity in C57BL/6J mice first made obese by 107 days of HF feeding. In contrast to our preventative study, we found that already obese mice did not tolerate mitoQ at 500 μmol/L...
April 2017: Pharmacology Research & Perspectives
https://www.readbyqxmd.com/read/28248600/mitochondria-targeted-antioxidant-mitoquinone-reduces-cisplatin-induced-ototoxicity-in-guinea-pigs
#13
Alan D Tate, Patrick J Antonelli, Kyle R Hannabass, Carolyn O Dirain
Objective To determine if mitoquinone (MitoQ) attenuates cisplatin-induced hearing loss in guinea pigs. Study Design Prospective and controlled animal study. Setting Academic, tertiary medical center. Subjects and Methods Guinea pigs were injected subcutaneously with either 5 mg/kg MitoQ (n = 9) or normal saline (control, n = 9) for 7 days and 1 hour before receiving a single dose of 10 mg/kg cisplatin. Auditory brainstem response thresholds were measured before MitoQ or saline administration and 3 to 4 days after cisplatin administration...
March 2017: Otolaryngology—Head and Neck Surgery
https://www.readbyqxmd.com/read/28121478/mitoq-regulates-autophagy-by-inducing-a-pseudo-mitochondrial-membrane-potential
#14
Chao Sun, Xiongxiong Liu, Cuixia Di, Zhenhua Wang, Xiangquan Mi, Yang Liu, Qiuyue Zhao, Aihong Mao, Weiqiang Chen, Lu Gan, Hong Zhang
During the process of oxidative phosphorylation, protons are pumped into the mitochondrial intermembrane space to establish a mitochondrial membrane potential (MMP). The electrochemical gradient generated allows protons to return to the matrix through the ATP synthase complex and generates ATP in the process. MitoQ is a lipophilic cationic drug that is adsorbed to the inner mitochondrial membrane; however, the cationic moiety of MitoQ remains in the intermembrane space. We found that the positive charges in MitoQ inhibited the activity of respiratory chain complexes I, III, and IV, reduced proton production, and decreased oxygen consumption...
April 3, 2017: Autophagy
https://www.readbyqxmd.com/read/28050775/neuroprotective-efficacy-of-mitochondrial-antioxidant-mitoq-in-suppressing-peroxynitrite-mediated-mitochondrial-dysfunction-inflicted-by-lead-toxicity-in-the-rat-brain
#15
Arpan Kumar Maiti, Nimai Chandra Saha, Sunil S More, Ashish Kumar Panigrahi, Goutam Paul
Lead (Pb) is one of the most pollutant metals that accumulate in the brain mitochondria disrupting mitochondrial structure and function. Though oxidative stress mediated by reactive oxygen species remains the most accepted mechanism of Pb neurotoxicity, some reports suggest the involvement of nitric oxide ((•)NO) and reactive nitrogen species in Pb-induced neurotoxicity. But the impact of Pb neurotoxicity on mitochondrial respiratory enzyme complexes remains unknown with no relevant report highlighting the involvement of peroxynitrite (ONOO(-)) in it...
April 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28034666/oxidative-stress-in-sepsis-pathophysiological-implications-justifying-antioxidant-co-therapy
#16
REVIEW
Carlos André Prauchner
Sepsis is one of the main causes of death among critically ill patients. Sepsis pathogenesis includes infection by gram-negative and gram-positive bacteria, fungi, or both; exacerbated inflammatory response; hypotension, with potential to cause vasodilatory shock; and lesser delivery of oxygen to tissues due to impairment of oxygen utilization by cells. The participation of reactive species and/or free radicals such as nitric oxide (NO), peroxynitrite (ONOO(-)), superoxide (O2(-)), hydrogen peroxide (H2O2), and hydroxyl radical (OH) has been reported to underlie these effects...
May 2017: Burns: Journal of the International Society for Burn Injuries
https://www.readbyqxmd.com/read/28033563/the-mitochondria-targeted-antioxidant-mitoq-ameliorated-tubular-injury-mediated-by-mitophagy-in-diabetic-kidney-disease-via-nrf2-pink1
#17
Li Xiao, Xiaoxuan Xu, Fan Zhang, Ming Wang, Yan Xu, Dan Tang, Jiahui Wang, Yan Qin, Yu Liu, Chengyuan Tang, Liyu He, Anna Greka, Zhiguang Zhou, Fuyou Liu, Zheng Dong, Lin Sun
Mitochondria play a crucial role in tubular injury in diabetic kidney disease (DKD). MitoQ is a mitochondria-targeted antioxidant that exerts protective effects in diabetic mice, but the mechanism underlying these effects is not clear. We demonstrated that mitochondrial abnormalities, such as defective mitophagy, mitochondrial reactive oxygen species (ROS) overexpression and mitochondrial fragmentation, occurred in the tubular cells of db/db mice, accompanied by reduced PINK and Parkin expression and increased apoptosis...
April 2017: Redox Biology
https://www.readbyqxmd.com/read/28030582/therapeutic-targeting-of-the-mitochondria-initiates-excessive-superoxide-production-and-mitochondrial-depolarization-causing-decreased-mtdna-integrity
#18
Kaytee L Pokrzywinski, Thomas G Biel, Dmitry Kryndushkin, V Ashutosh Rao
Mitochondrial dysregulation is closely associated with excessive reactive oxygen species (ROS) production. Altered redox homeostasis has been implicated in the onset of several diseases including cancer. Mitochondrial DNA (mtDNA) and proteins are particularly sensitive to ROS as they are in close proximity to the respiratory chain (RC). Mitoquinone (MitoQ), a mitochondria-targeted redox agent, selectively damages breast cancer cells possibly through damage induced via enhanced ROS production. However, the effects of MitoQ and other triphenylphosphonium (TPP+) conjugated agents on cancer mitochondrial homeostasis remain unknown...
2016: PloS One
https://www.readbyqxmd.com/read/27930931/deficiency-in-duox2-activity-alleviates-ileitis-in-gpx1-and-gpx2-knockout-mice-without-affecting-apoptosis-incidence-in-the-crypt-epithelium
#19
Fong-Fong Chu, R Steven Esworthy, James H Doroshow, Helmut Grasberger, Agnes Donko, Thomas L Leto, Qiang Gao, Binghui Shen
Mice deficient in glutathione peroxidase (GPx)-1 and -2 (GPx1(-/-)GPx2(-/-) double knockout or DKO mice) develop very-early-onset (VEO) ileocolitis, suggesting that lack of defense against reactive oxygen species (ROS) renders susceptibility to intestinal inflammation. Two members of ROS-generating NADPH oxidase family, NOX1 and DUOX2, are highly inducible in the intestinal epithelium. Previously, we reported that Nox1 deficiency ameliorated the pathology in DKO mice (Nox1-TKO). The role of Duox2 in ileocolitis of the DKO mice is evaluated here in Duoxa-TKO mice by breeding DKO mice with Duoxa(-/-) mice (Duoxa-TKO), which do not have Duox2 activity...
April 2017: Redox Biology
https://www.readbyqxmd.com/read/27922686/necrox-5-prevents-breast-cancer-metastasis-by-akt-inhibition-via-reducing-intracellular-calcium-levels
#20
Jin-Hee Park, Hyoung Kyu Kim, Hana Jung, Ki Hyang Kim, Mi Seon Kang, Jun Hyuk Hong, Byeng Chul Yu, Sungjae Park, Su-Kil Seo, Il Whan Choi, Soon Ha Kim, Nari Kim, Jin Han, Sae Gwang Park
A major goal of breast cancer research is to prevent the molecular events that lead to tumour metastasis. It is well-established that both cytoplasmic and mitochondrial reactive oxygen species (ROS) play important roles in cell migration and metastasis. Accordingly, this study examined the molecular mechanisms of the anti-metastatic effects of NecroX-5, a mitochondrial ROS scavenger. NecroX-5 inhibited lung cancer metastasis by ameliorating migration in a mouse model. In human cancer cells, the inhibition of migration by NecroX-5 is cell type-dependent...
January 2017: International Journal of Oncology
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