Losartan decreases cardiac muscle fibrosis and improves cardiac function in dystrophin-deficient mdx mice. - Wikidata - awgldk - TriplyDB

Losartan decreases cardiac muscle fibrosis and improves cardiac function in dystrophin-deficient mdx mice.

Losartan decreases cardiac muscle fibrosis and improves cardiac function in dystrophin-deficient mdx mice.

http://www.wikidata.org/entity/Q34103278

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Current and emerging treatment strategies for Duchenne muscular dystrophy Therapeutic strategies for preventing skeletal muscle fibrosis after injury Proteomic profiling of the dystrophin-deficient mdx phenocopy of dystrophinopathy-associated cardiomyopathy Current understanding of molecular pathology and treatment of cardiomyopathy in duchenne muscular dystrophy Speckle tracking analysis of the left ventricular anterior wall shows significantly decreased relative radial strain patterns in dystrophin deficient mice after 9 months of age Novel approach to meta-analysis of microarray datasets reveals muscle remodeling-related drug targets and biomarkers in Duchenne muscular dystrophy Magnetic Resonance Imaging Is Sensitive to Pathological Amelioration in a Model for Laminin-Deficient Congenital Muscular Dystrophy (MDC1A)A randomized, double-blind trial of lisinopril and losartan for the treatment of cardiomyopathy in duchenne muscular dystrophy.Biochemical and Functional Comparisons of mdx and Sgcg(-/-) Muscular Dystrophy Mouse Models.Targeting TGF-β Signaling by Antisense Oligonucleotide-mediated Knockdown of TGF-β Type I Receptor.Membrane sealant Poloxamer P188 protects against isoproterenol induced cardiomyopathy in dystrophin deficient mice.Chronic losartan administration reduces mortality and preserves cardiac but not skeletal muscle function in dystrophic mice.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials Omigapil treatment decreases fibrosis and improves respiratory rate in dy(2J) mouse model of congenital muscular dystrophy High throughput screening in duchenne muscular dystrophy: from drug discovery to functional genomics Prednisolone attenuates improvement of cardiac and skeletal contractile function and histopathology by lisinopril and spironolactone in the mdx mouse model of Duchenne muscular dystrophy.Sarcolemma instability during mechanical activity in Largemyd cardiac myocytes with loss of dystroglycan extracellular matrix receptor function Role of TGF-β signaling in inherited and acquired myopathies.Evaluation of 11C-acetate and 18F-FDG PET/CT in mouse multidrug resistance gene-2 deficient mouse model of hepatocellular carcinoma.Angiotensin-dependent autonomic dysregulation precedes dilated cardiomyopathy in a mouse model of muscular dystrophy.The Effects of Experimental Sleep Apnea on Cardiac and Respiratory Functions in 6 and 18 Month Old Dystrophic (mdx) Mice.Inhibition of inflammation with celastrol fails to improve muscle function in dysferlin-deficient A/J mice Matrix-dependent perturbation of TGFβ signaling and disease Δ-9,11 modification of glucocorticoids dissociates nuclear factor-κB inhibitory efficacy from glucocorticoid response element-associated side effects.Emerging drugs for Duchenne muscular dystrophy Vascular-targeted therapies for Duchenne muscular dystrophy Conditional expression of TGF-β1 in skeletal muscles causes endomysial fibrosis and myofibers atrophy Angiotensin receptor blockade mediated amelioration of mucopolysaccharidosis type I cardiac and craniofacial pathology.Cardiomyopathy of Duchenne muscular dystrophy: current understanding and future directions.LOX-1 and angiotensin receptors, and their interplay.Cell-matrix interactions in muscle disease.Treatment of dystrophinopathic cardiomyopathy: review of the literature and personal results.Cardiac and respiratory dysfunction in Duchenne muscular dystrophy and the role of second messengers.Treatment of dystrophin cardiomyopathies.Prospect for pharmacological therapies to treat skeletal muscle dysfunction.Renin-angiotensin system: an old player with novel functions in skeletal muscle.Connective tissue regeneration in skeletal muscle after eccentric contraction-induced injury.Pharmacological therapeutics targeting the secondary defects and downstream pathology of Duchenne muscular dystrophy Angiotensin II type 1 receptor antagonists alleviate muscle pathology in the mouse model for laminin-α2-deficient congenital muscular dystrophy (MDC1A).Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy

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Losartan decreases cardiac muscle fibrosis and improves cardiac function in dystrophin-deficient mdx mice.

http://www.wikidata.org/entity/Q34103278

description

2011 nî lūn-bûn

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2011 թուականի Մարտին հրատարակուած գիտական յօդուած

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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type

label

Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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prefLabel

Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Journal of Cardiovascular Pharmacology and Therapeutics

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Losartan decreases cardiac mus ...... dystrophin-deficient mdx mice.

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Alfredo D Guerron

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Arpana Sali

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Christopher F Spurney

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Eric P Hoffman

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Heather Gordish-Dressman

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Jack van der Meulen

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Micaela Iantorno

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Qing Yu

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Sree Rayavarapu

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P2860

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 G

Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome

Angiotensin II blockade reverses myocardial fibrosis in a transgenic mouse model of human hypertrophic cardiomyopathy

Modulation of disease severity in mice with targeted disruption of the acid alpha-glucosidase gene

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Non-Smad pathways in TGF-beta signaling

Evaluation of skeletal and cardiac muscle function after chronic administration of thymosin beta-4 in the dystrophin deficient mouse.

Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies

Preclinical drug trials in the mdx mouse: assessment of reliable and sensitive outcome measures.

Angiotensin II type 1 receptor blockade attenuates TGF-beta-induced failure of muscle regeneration in multiple myopathic states.

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87-95

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1

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Kanneboyina Nagaraju

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49820136

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21304057

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