The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model. - Wikidata - awgldk - TriplyDB

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

http://www.wikidata.org/entity/Q34790975

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Allele-specific silencing of mutant Myh6 transcripts in mice suppresses hypertrophic cardiomyopathy Hypertrophic cardiomyopathy in childhood Myosin binding protein C: implications for signal-transduction The physiology of cardiovascular disease and innovative liposomal platforms for therapy Genetic considerations in hypertrophic cardiomyopathy Targets for therapy in sarcomeric cardiomyopathies Fibroblast growth factor receptor 1 signaling in adult cardiomyocytes increases contractility and results in a hypertrophic cardiomyopathy Genetics and disease of ventricular muscle.Research priorities in sarcomeric cardiomyopathies Calsequestrin 2 (CASQ2) mutations increase expression of calreticulin and ryanodine receptors, causing catecholaminergic polymorphic ventricular tachycardia Study familial hypertrophic cardiomyopathy using patient-specific induced pluripotent stem cells Abnormal calcium handling properties underlie familial hypertrophic cardiomyopathy pathology in patient-specific induced pluripotent stem cells Combinatorial effects of double cardiomyopathy mutant alleles in rodent myocytes: a predictive cellular model of myofilament dysregulation in disease Cardiac myosin missense mutations cause dilated cardiomyopathy in mouse models and depress molecular motor function.Echocardiographic strain imaging to assess early and late consequences of sarcomere mutations in hypertrophic cardiomyopathy Diastolic dysfunction and thin filament dysregulation resulting from excitation-contraction uncoupling in a mouse model of restrictive cardiomyopathy.Sexually dimorphic myofilament function and cardiac troponin I phosphospecies distribution in hypertrophic cardiomyopathy mice Deletion of the β2-adrenergic receptor prevents the development of cardiomyopathy in mice.Modeling structural and functional deficiencies of RBM20 familial dilated cardiomyopathy using human induced pluripotent stem cells Genetic causes of human heart failure.Rescue of familial cardiomyopathies by modifications at the level of sarcomere and Ca2+ fluxes.Ablation of LKB1 in the heart leads to energy deprivation and impaired cardiac function.Differential activation of stress-response signaling in load-induced cardiac hypertrophy and failure.Experimental therapies in hypertrophic cardiomyopathy Tissue Doppler imaging predicts the development of hypertrophic cardiomyopathy in subjects with subclinical disease.Hypertrophic cardiomyopathy: a heart in need of an energy bar?Genetics of hypertrophic cardiomyopathy.Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β.Somatic events modify hypertrophic cardiomyopathy pathology and link hypertrophy to arrhythmia.Reversibility of PRKAG2 glycogen-storage cardiomyopathy and electrophysiological manifestations.Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy.T-cadherin is critical for adiponectin-mediated cardioprotection in mice.Narrative review: harnessing molecular genetics for the diagnosis and management of hypertrophic cardiomyopathy.Genetic testing for potentially lethal, highly treatable inherited cardiomyopathies/channelopathies in clinical practice.Drug screening using a library of human induced pluripotent stem cell-derived cardiomyocytes reveals disease-specific patterns of cardiotoxicity Beyond the sarcomere: CSRP3 mutations cause hypertrophic cardiomyopathy.Genetics and clinical destiny: improving care in hypertrophic cardiomyopathy Diltiazem treatment for pre-clinical hypertrophic cardiomyopathy sarcomere mutation carriers: a pilot randomized trial to modify disease expression.Hypertrophic cardiomyopathy: from gene defect to clinical disease.Altered myocardial calcium cycling and energetics in heart failure--a rational approach for disease treatment.

P2860

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P2860

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

http://www.wikidata.org/entity/Q34790975

description

2002 nî lūn-bûn

@nan

2002 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2002 թվականի ապրիլին հրատարակված գիտական հոդված

@hy

2002年の論文

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2002年論文

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2002年論文

@zh-hant

2002年論文

@zh-hk

2002年論文

@zh-mo

2002年論文

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2002年论文

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name

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@ast

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@en

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@nl

type

label

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@ast

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@en

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@nl

prefLabel

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@ast

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@en

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@nl

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P1433

Journal of Clinical Investigation

P1476

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

@en

P2093

Andrew R Marks

http://www.w3.org/2001/XMLSchema#string

Bradley K McConnell

http://www.w3.org/2001/XMLSchema#string

Christine E Seidman

http://www.w3.org/2001/XMLSchema#string

David A Kass

http://www.w3.org/2001/XMLSchema#string

Dimitrios Georgakopoulos

http://www.w3.org/2001/XMLSchema#string

Imran Ahmad

http://www.w3.org/2001/XMLSchema#string

J G Seidman

http://www.w3.org/2001/XMLSchema#string

Joachim P Schmitt

http://www.w3.org/2001/XMLSchema#string

Michael Giewat

http://www.w3.org/2001/XMLSchema#string

Steven Reiken

http://www.w3.org/2001/XMLSchema#string

P2860

Neonatal cardiomyopathy in mice homozygous for the Arg403Gln mutation in the alpha cardiac myosin heavy chain gene.

PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts

Calcium fluxes involved in control of cardiac myocyte contraction

Complex formation between junctin, triadin, calsequestrin, and the ryanodine receptor. Proteins of the cardiac junctional sarcoplasmic reticulum membrane

Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy

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

Dilated cardiomyopathy in homozygous myosin-binding protein-C mutant mice

Altered crossbridge kinetics in the alphaMHC403/+ mouse model of familial hypertrophic cardiomyopathy

Distribution of proteins implicated in excitation-contraction coupling in rat ventricular myocytes

A polymorphic modifier gene alters the hypertrophic response in a murine model of familial hypertrophic cardiomyopathy

P304

1013-1020

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scholarly article

P356

10.1172/JCI200214677

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P407

P433

8

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P478

109

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P50

Christopher Semsarian

P577

2002-04-01T00:00:00Z

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P698

11956238

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P932

150949

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