Chronic losartan administration reduces mortality and preserves cardiac but not skeletal muscle function in dystrophic mice. - Wikidata - wikimedia - TriplyDB

Chronic losartan administration reduces mortality and preserves cardiac but not skeletal muscle function in dystrophic mice.

Chronic losartan administration reduces mortality and preserves cardiac but not skeletal muscle function in dystrophic mice.

http://www.wikidata.org/entity/Q33952122

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Current and emerging treatment strategies for 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.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials 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.Angiotensin-dependent autonomic dysregulation precedes dilated cardiomyopathy in a mouse model of muscular dystrophy.Emerging drugs for Duchenne muscular dystrophy Vascular-targeted therapies for Duchenne muscular dystrophy Long-term wheel running compromises diaphragm function but improves cardiac and plantarflexor function in the mdx mouse The angiotensin receptor blocker, Losartan, inhibits mammary tumor development and progression to invasive carcinoma.Treatment of dystrophinopathic cardiomyopathy: review of the literature and personal results.Treatment of dystrophin cardiomyopathies.Inhibition of the renin-angiotensin system improves physiological outcomes in mice with mild or severe cancer cachexia.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).Understanding the process of fibrosis in Duchenne muscular dystrophy.Myocardial fibrosis burden predicts left ventricular ejection fraction and is associated with age and steroid treatment duration in duchenne muscular dystrophy Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat.Suramin attenuates dystrophin-deficient cardiomyopathy in the mdx mouse model of duchenne muscular dystrophy.Inhibition of the angiotensin-converting enzyme decreases skeletal muscle fibrosis in dystrophic mice by a diminution in the expression and activity of connective tissue growth factor (CTGF/CCN-2).Cardiac characterization of mdx mice using high-resolution doppler echocardiography.Disruption of muscle renin-angiotensin system in AT1a-/- mice enhances muscle function despite reducing muscle mass but compromises repair after injury.

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Chronic losartan administration reduces mortality and preserves cardiac but not skeletal muscle function in dystrophic mice.

http://www.wikidata.org/entity/Q33952122

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2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2011 թվականի հունիսին 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

Chronic losartan administratio ...... e function in dystrophic mice.

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Chronic losartan administratio ...... e function in dystrophic mice.

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Chronic losartan administratio ...... e function in dystrophic mice.

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Chronic losartan administratio ...... e function in dystrophic mice.

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Chronic losartan administratio ...... e function in dystrophic mice.

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Elisabeth R Barton

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H Lee Sweeney

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Jeffrey A Gazzara

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Kevin J Morine

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Lawrence T Bish

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Mark Yarchoan

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Meg M Sleeper

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Pedro Acosta

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P2860

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

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

TGF-beta signaling and the fibrotic response

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

Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β.

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

Approaching a new age in Duchenne muscular dystrophy treatment.

Duchenne muscular dystrophy and dystrophin: pathogenesis and opportunities for treatment

Prognostic implications of qualitative assessment of left ventricular function compared to simple routine quantitative echocardiography

Gene therapy in heart failure.

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10.1371/JOURNAL.PONE.0020856

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