Early treatment with lisinopril and spironolactone preserves cardiac and skeletal muscle in Duchenne muscular dystrophy mice.
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The role of fibrosis in Duchenne muscular dystrophyHomologous recombination mediates functional recovery of dysferlin deficiency following AAV5 gene transferRationally engineered Troponin C modulates in vivo cardiac function and performance in health and diseaseAnimal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapyLosartan Treatment Protects Retinal Ganglion Cells and Alters Scleral Remodeling in Experimental GlaucomaSmall and large animal models in cardiac contraction research: advantages and disadvantagesPharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trialsRationale for treating oedema in Duchenne muscular dystrophy with eplerenoneDystrobrevin increases dystrophin's binding to the dystrophin-glycoprotein complex and provides protection during cardiac stressPrednisolone attenuates improvement of cardiac and skeletal contractile function and histopathology by lisinopril and spironolactone in the mdx mouse model of Duchenne muscular dystrophy.Eplerenone for early cardiomyopathy in Duchenne muscular dystrophy: a randomised, double-blind, placebo-controlled trialAAV.Dysferlin Overlap Vectors Restore Function in Dysferlinopathy Animal ModelsDefective membrane fusion and repair in Anoctamin5-deficient muscular dystrophy.Contemporary cardiac issues in Duchenne muscular dystrophy. Working Group of the National Heart, Lung, and Blood Institute in collaboration with Parent Project Muscular Dystrophy.In vivo assessment of contractile strength distinguishes differential gene function in skeletal muscle of zebrafish larvae.Mineralocorticoid receptors are present in skeletal muscle and represent a potential therapeutic target.Cardiomyopathy in the dystrophin/utrophin-deficient mouse model of severe muscular dystrophy is characterized by dysregulation of matrix metalloproteinases.The force-temperature relationship in healthy and dystrophic mouse diaphragm; implications for translational study design.Duchenne Muscular Dystrophy Mice and Men: Can Understanding a Genetic Cardiomyopathy Inform Treatment of Other Myocardial Diseases?The Angiotensin Converting Enzyme Inhibitor Lisinopril Improves Muscle Histopathology but not Contractile Function in a Mouse Model of Duchenne Muscular Dystrophy.Aldosterone, mineralocorticoid receptor activation, and cardiovascular remodeling.Childhood ataxia: clinical features, pathogenesis, key unanswered questions, and future directions.Muscle damage, metabolism, and oxidative stress in mdx mice: Impact of aerobic runningSimilar efficacy from specific and non-specific mineralocorticoid receptor antagonist treatment of muscular dystrophy mice.Myocardial Contractile Dysfunction Is Present without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and Is Prevented after Claudin-5 Virotherapy.Prevalence and distribution of late gadolinium enhancement in a large population of patients with Duchenne muscular dystrophy: effect of age and left ventricular systolic function.Wnt protein-mediated satellite cell conversion in adult and aged mice following voluntary wheel running.Eplerenone for early cardiomyopathy in Duchenne muscular dystrophy: results of a two-year open-label extension trialUpdate on the treatment of Duchenne muscular dystrophy.Cardiac and respiratory dysfunction in Duchenne muscular dystrophy and the role of second messengers.The physiological response of protease inhibition in dystrophic muscle.Treatment of dystrophin cardiomyopathies.Gene expression effects of glucocorticoid and mineralocorticoid receptor agonists and antagonists on normal human skeletal muscle.Regulation of NADPH oxidases in skeletal muscle.High field magnetic resonance imaging of rodents in cardiovascular research.Renin-angiotensin-aldosterone system inhibitors improve membrane stability and change gene-expression profiles in dystrophic skeletal muscles.Understanding the process of fibrosis in Duchenne muscular dystrophy.Systemic AAV-Mediated β-Sarcoglycan Delivery Targeting Cardiac and Skeletal Muscle Ameliorates Histological and Functional Deficits in LGMD2E Mice.Myocardial fibrosis burden predicts left ventricular ejection fraction and is associated with age and steroid treatment duration in duchenne muscular dystrophyDuchenne muscular dystrophy fibroblast nodules: a cell-based assay for screening anti-fibrotic agents.
P2860
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P2860
Early treatment with lisinopril and spironolactone preserves cardiac and skeletal muscle in Duchenne muscular dystrophy mice.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Early treatment with lisinopri ...... henne muscular dystrophy mice.
@en
Early treatment with lisinopri ...... henne muscular dystrophy mice.
@nl
type
label
Early treatment with lisinopri ...... henne muscular dystrophy mice.
@en
Early treatment with lisinopri ...... henne muscular dystrophy mice.
@nl
prefLabel
Early treatment with lisinopri ...... henne muscular dystrophy mice.
@en
Early treatment with lisinopri ...... henne muscular dystrophy mice.
@nl
P2093
P2860
P1433
P1476
Early treatment with lisinopri ...... chenne muscular dystrophy mice
@en
P2093
Benjamin D Canan
Christopher D Martin
Dawn A Delfín
Jason D Murray
Jenna E Stangland
Jill A Rafael-Fortney
Kevin E Schill
Neeraj S Chimanji
Ranjit Ganguly
Subha V Raman
P2860
P304
P356
10.1161/CIRCULATIONAHA.111.031716
P407
P577
2011-07-18T00:00:00Z