Oxidative stress by monoamine oxidases is causally involved in myofiber damage in muscular dystrophy. - Wikidata - awgldk - TriplyDB

Oxidative stress by monoamine oxidases is causally involved in myofiber damage in muscular dystrophy.

Oxidative stress by monoamine oxidases is causally involved in myofiber damage in muscular dystrophy.

http://www.wikidata.org/entity/Q42934854

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Activation of autophagy is required for muscle homeostasis during physical exercise Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches Pharmacology and Clinical Drug Candidates in Redox Medicine Reactive Oxygen-Related Diseases: Therapeutic Targets and Emerging Clinical Indications Early pathogenesis of Duchenne muscular dystrophy modelled in patient-derived human induced pluripotent stem cells.Molecular Insights into Human Monoamine Oxidase B Inhibition by the Glitazone Antidiabetes Drugs Mitochondrial Metabolism in Aging Heart Skeletal muscle NADPH oxidase is increased and triggers stretch-induced damage in the mdx mouse.Molecular diagnosis of duchenne muscular dystrophy: past, present and future in relation to implementing therapies Monoamine oxidase inhibition prevents mitochondrial dysfunction and apoptosis in myoblasts from patients with collagen VI myopathies.Altered cross-bridge properties in skeletal muscle dystrophies A platelet protein biochip rapidly detects an Alzheimer's disease-specific phenotype Melanocytes from Patients Affected by Ullrich Congenital Muscular Dystrophy and Bethlem Myopathy have Dysfunctional Mitochondria That Can be Rescued with Cyclophilin Inhibitors.Emerging importance of oxidative stress in regulating striated muscle elasticity.Protective effects of Arctium lappa L. roots against hydrogen peroxide-induced cell injury and potential mechanisms in SH-SY5Y cells.Potent organo-osmium compound shifts metabolism in epithelial ovarian cancer cells.Melanocytes--a novel tool to study mitochondrial dysfunction in Duchenne muscular dystrophy.Novel compounds for the treatment of Duchenne muscular dystrophy: emerging therapeutic agents Concepts of scientific integrative medicine applied to the physiology and pathophysiology of catecholamine systems.Mitochondrial alterations and oxidative stress in an acute transient mouse model of muscle degeneration: implications for muscular dystrophy and related muscle pathologies.Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation.The dystrophin-glycoprotein complex in the prevention of muscle damage.Redox control of NLRP3 inflammasome activation in health and disease.Nuclear damages and oxidative stress: new perspectives for laminopathies.Oxidative stress in muscular dystrophy: from generic evidence to specific sources and targets.Autophagy in skeletal muscle homeostasis and in muscular dystrophies Sialic acid deficiency is associated with oxidative stress leading to muscle atrophy and weakness in GNE myopathy.Proteomic and transcriptomic analysis of heart failure due to volume overload in a rat aorto-caval fistula model provides support for new potential therapeutic targets - monoamine oxidase A and transglutaminase 2.Muscle biopsies from human muscle diseases with myopathic pathology reveal common alterations in mitochondrial function.Increased NLRP3-dependent interleukin 1β secretion in patients with familial Mediterranean fever: correlation with MEFV genotype.Lack of collagen VI promotes neurodegeneration by impairing autophagy and inducing apoptosis during aging.Correlation between circulating corticosterone and protein carbonylation in the liver after short-term hypokinesia.Oxidative stress, NF-κB and the ubiquitin proteasomal pathway in the pathology of calpainopathy.Quantum-chemical approach to determining the high potency of clorgyline as an irreversible acetylenic monoamine oxidase inhibitor.Effect of some pyrimidine compounds on rat brain monoamine oxidase-B in vitro.Exosome-Mediated Benefits of Cell Therapy in Mouse and Human Models of Duchenne Muscular Dystrophy.Utrophin A is essential in mediating the functional adaptations of mdx mouse muscle following chronic AMPK activation.Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies.Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype in Mice and in Myogenic Cultures From DMD Patients

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Oxidative stress by monoamine oxidases is causally involved in myofiber damage in muscular dystrophy.

http://www.wikidata.org/entity/Q42934854

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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2010年论文

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name

Oxidative stress by monoamine ...... damage in muscular dystrophy.

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Oxidative stress by monoamine ...... damage in muscular dystrophy.

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Oxidative stress by monoamine ...... damage in muscular dystrophy.

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Oxidative stress by monoamine ...... damage in muscular dystrophy.

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Oxidative stress by monoamine ...... damage in muscular dystrophy.

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Oxidative stress by monoamine ...... damage in muscular dystrophy.

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Human Molecular Genetics

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Oxidative stress by monoamine ...... damage in muscular dystrophy.

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P2093

Barbara Spolaore

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Carlo Reggiani

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Marcella Canton

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Paolo Bonaldo

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Sara Menazza

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Tania Tiepolo

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P2860

Investigation of Debio 025, a cyclophilin inhibitor, in the dystrophic mdx mouse, a model for Duchenne muscular dystrophy

Cyclosporin A corrects mitochondrial dysfunction and muscle apoptosis in patients with collagen VI myopathies

Cell Therapy of -Sarcoglycan Null Dystrophic Mice Through Intra-Arterial Delivery of Mesoangioblasts

Protein oxidation in aging, disease, and oxidative stress

Monoamine oxidase A-mediated enhanced catabolism of norepinephrine contributes to adverse remodeling and pump failure in hearts with pressure overload.

Physiological consequences of tropomyosin mutations associated with cardiac and skeletal myopathies.

Muscular dystrophies involving the dystrophin-glycoprotein complex: an overview of current mouse models.

Oxidative stress and the pathogenesis of muscular dystrophies.

Mitochondrial dysfunction in the pathogenesis of Ullrich congenital muscular dystrophy and prospective therapy with cyclosporins

Integrins engage mitochondrial function for signal transduction by a mechanism dependent on Rho GTPases.

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4207-4215

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scholarly article

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10.1093/HMG/DDQ339

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21

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19

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Paola Braghetta

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2010-08-17T00:00:00Z

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45694606

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20716577

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