Metabolic remodeling agents show beneficial effects in the dystrophin-deficient mdx mouse model - Wikidata - wikimedia - TriplyDB

Metabolic remodeling agents show beneficial effects in the dystrophin-deficient mdx mouse model

Metabolic remodeling agents show beneficial effects in the dystrophin-deficient mdx mouse model

http://www.wikidata.org/entity/Q36351079

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Metformin protects skeletal muscle from cardiotoxin induced degeneration Non-invasive MRI and spectroscopy of mdx mice reveal temporal changes in dystrophic muscle imaging and in energy deficits Metabolic dysfunction and altered mitochondrial dynamics in the utrophin-dystrophin deficient mouse model of duchenne muscular dystrophy Metformin to Augment Strength Training Effective Response in Seniors (MASTERS): study protocol for a randomized controlled trial.Exercise-induced skeletal muscle remodeling and metabolic adaptation: redox signaling and role of autophagy.Resveratrol induces expression of the slow, oxidative phenotype in mdx mouse muscle together with enhanced activity of the SIRT1-PGC-1α axis.Activation of the ubiquitin proteasome pathway in a mouse model of inflammatory myopathy: a potential therapeutic target Divergent modification of low-dose ⁵⁶Fe-particle and proton radiation on skeletal muscle Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials Hyperhomocysteinemia associated skeletal muscle weakness involves mitochondrial dysfunction and epigenetic modifications.Muscular dystrophy in the mdx mouse is a severe myopathy compounded by hypotrophy, hypertrophy and hyperplasia.Improved Muscle Function in Duchenne Muscular Dystrophy through L-Arginine and Metformin: An Investigator-Initiated, Open-Label, Single-Center, Proof-Of-Concept-Study.Dystrophin-glycoprotein complex regulates muscle nitric oxide production through mechanoregulation of AMPK signaling Development of autoantibodies against muscle-specific FHL1 in severe inflammatory myopathies.Combinatorial therapeutic activation with heparin and AICAR stimulates additive effects on utrophin A expression in dystrophic muscles.Chronic Treatment with the AMPK Agonist AICAR Prevents Skeletal Muscle Pathology but Fails to Improve Clinical Outcome in a Mouse Model of Severe Spinal Muscular Atrophy.Identification of disease specific pathways using in vivo SILAC proteomics in dystrophin deficient mdx mouse.In Vitro and In Vivo Modulation of Alternative Splicing by the Biguanide Metformin Skeletal muscle fiber type: using insights from muscle developmental biology to dissect targets for susceptibility and resistance to muscle disease.Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophy.Mitochondria mediate cell membrane repair and contribute to Duchenne muscular dystrophy.Turn up the power - pharmacological activation of mitochondrial biogenesis in mouse models.Role of Toll-like receptors in the pathogenesis of dystrophin-deficient skeletal and heart muscle Increased AMP-activated protein kinase in skeletal muscles of Murphy Roth Large mice and its potential role in altered metabolism.Dystrophin induced cognitive impairment: mechanisms, models and therapeutic strategies Activation of AMPK and its Impact on Exercise Capacity.Novel investigational drugs mimicking exercise for the treatment of cachexia.Regulation of myoblast differentiation by metabolic perturbations induced by metformin.Sustained AMPK activation improves muscle function in a mitochondrial myopathy mouse model by promoting muscle fiber regeneration.Post-natal induction of PGC-1α protects against severe muscle dystrophy independently of utrophin.The mitochondrial metabolic reprogramming agent trimetazidine as an 'exercise mimetic' in cachectic C26-bearing mice.AMPK in skeletal muscle function and metabolism.Alteration in CatSper1 and 2 genes expression, sperm parameters and testis histology in varicocelized rats.Utrophin A is essential in mediating the functional adaptations of mdx mouse muscle following chronic AMPK activation.At the Crossroads of Clinical and Preclinical Research for Muscular Dystrophy-Are We Closer to Effective Treatment for Patients?Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies.

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Metabolic remodeling agents show beneficial effects in the dystrophin-deficient mdx mouse model

http://www.wikidata.org/entity/Q36351079

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Metabolic remodeling agents sh ...... phin-deficient mdx mouse model

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Skeletal Muscle

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Eric P Hoffman

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Helen K Johnston

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Jack H Van Der Meulen

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Terrence Partridge

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Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha): transcriptional coactivator and metabolic regulator

miR-31 modulates dystrophin expression: new implications for Duchenne muscular dystrophy therapy

Peroxisome proliferator-activated receptor gamma coactivator 1alpha or 1beta overexpression inhibits muscle protein degradation, induction of ubiquitin ligases, and disuse atrophy

AMPK and PPARdelta agonists are exercise mimetics

Regulation of muscle fiber type and running endurance by PPARdelta

Rescue of dystrophic skeletal muscle by PGC-1α involves a fast to slow fiber type shift in the mdx mouse

Daily treatment with SMTC1100, a novel small molecule utrophin upregulator, dramatically reduces the dystrophic symptoms in the mdx mouse

Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy

PPARδ regulates satellite cell proliferation and skeletal muscle regeneration

Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression

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10.1186/2044-5040-2-16

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1

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Kanneboyina Nagaraju

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