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Targets for therapy in sarcomeric cardiomyopathies

Targets for therapy in sarcomeric cardiomyopathies

http://www.wikidata.org/entity/Q27027023

about

Novel myosin-based therapies for congenital cardiac and skeletal myopathies Mutation-Specific Phenotypes in hiPSC-Derived Cardiomyocytes Carrying Either Myosin-Binding Protein C Or α-Tropomyosin Mutation for Hypertrophic Cardiomyopathy.Research priorities in sarcomeric cardiomyopathies Epigallocatechin-3-Gallate Accelerates Relaxation and Ca2+ Transient Decay and Desensitizes Myofilaments in Healthy and Mybpc3-Targeted Knock-in Cardiomyopathic Mice.Current perspectives in hypertrophic cardiomyopathy with the focus on patients in the Finnish population: a review.Modulating Beta-Cardiac Myosin Function at the Molecular and Tissue Levels.N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy.Molecular effects of the myosin activator omecamtiv mecarbil on contractile properties of skinned myocardium lacking cardiac myosin binding protein-C ADP-stimulated contraction: A predictor of thin-filament activation in cardiac disease.A Tension-Based Model Distinguishes Hypertrophic versus Dilated Cardiomyopathy.Preventing pediatric cardiomyopathy: a 2015 outlook.β-adrenergic receptor signalling and its functional consequences in the diseased heart.Linking myofilaments to sudden cardiac death: recent advances.Raf kinase inhibitor protein: lessons of a better way for β-adrenergic receptor activation in the heart.Pseudophosphorylation of cardiac myosin regulatory light chain: a promising new tool for treatment of cardiomyopathy.Myofilament protein dynamics modulate EAD formation in human hypertrophic cardiomyopathy.Selective phosphorylation of PKA targets after β-adrenergic receptor stimulation impairs myofilament function in Mybpc3-targeted HCM mouse model.Evaluation of MYBPC3 trans-Splicing and Gene Replacement as Therapeutic Options in Human iPSC-Derived Cardiomyocytes.Nebivolol Desensitizes Myofilaments of a Hypertrophic Cardiomyopathy Mouse Model.Pathogenesis of Hypertrophic Cardiomyopathy is Mutation Rather Than Disease Specific: A Comparison of the Cardiac Troponin T E163R and R92Q Mouse Models.Mechanisms of pro-arrhythmic abnormalities in ventricular repolarisation and anti-arrhythmic therapies in human hypertrophic cardiomyopathy.Life-long tailoring of management for patients with hypertrophic cardiomyopathy : Awareness and decision-making in changing scenarios.Which way to grow? Force over time may be the heart's Dao de jing.Diltiazem prevents stress-induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3-knock-in mice.Cardiovascular homeostasis dependence on MICU2, a regulatory subunit of the mitochondrial calcium uniporter.Contemporary genetic testing in inherited cardiac disease: tools, ethical issues, and clinical applications.The potential of obscurin as a therapeutic target in muscle disorders.Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effects in vivo in a mouse model of hypertrophic cardiomyopathy.Sarcomeric cardiomyopathies: from bedside to bench and back.Editorial highlights from Cardiovascular Research.Emerging pharmacologic and structural therapies for hypertrophic cardiomyopathy.Remodeling of repolarization and arrhythmia susceptibility in a myosin-binding protein C knockout mouse model.Molecular Defects in Cardiac Myofilament Ca2+-Regulation Due to Cardiomyopathy-Linked Mutations Can Be Reversed by Small Molecules Binding to Troponin.MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM from DCM.

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P2860

Targets for therapy in sarcomeric cardiomyopathies

http://www.wikidata.org/entity/Q27027023

description

2015 nî lūn-bûn

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2015 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2015 թվականի ապրիլին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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name

Targets for therapy in sarcomeric cardiomyopathies

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Targets for therapy in sarcomeric cardiomyopathies

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Targets for therapy in sarcomeric cardiomyopathies

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type

label

Targets for therapy in sarcomeric cardiomyopathies

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Targets for therapy in sarcomeric cardiomyopathies

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Targets for therapy in sarcomeric cardiomyopathies

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prefLabel

Targets for therapy in sarcomeric cardiomyopathies

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Targets for therapy in sarcomeric cardiomyopathies

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Targets for therapy in sarcomeric cardiomyopathies

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Cardiovascular Research

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Targets for therapy in sarcomeric cardiomyopathies

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Cecilia Ferrantini

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Corrado Poggesi

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Jil C Tardiff

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Lars S Maier

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Lucie Carrier

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Raffaele Coppini

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Sabine Huke

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P2860

Mutations in the gamma(2) subunit of AMP-activated protein kinase cause familial hypertrophic cardiomyopathy: evidence for the central role of energy compromise in disease pathogenesis

Alterations in thin filament regulation induced by a human cardiac troponin T mutant that causes dilated cardiomyopathy are distinct from those induced by troponin T mutants that cause hypertrophic cardiomyopathy

Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sites

Allele-specific silencing of mutant Myh6 transcripts in mice suppresses hypertrophic cardiomyopathy

Animal and in silico models for the study of sarcomeric cardiomyopathies

Pharmacological treatment options for hypertrophic cardiomyopathy: high time for evidence

Solution Structure of Human Cardiac Troponin C in Complex with the Green Tea Polyphenol, (-)-Epigallocatechin 3-Gallate

Solution structure of calmodulin-W-7 complex: the basis of diversity in molecular recognition

Single-molecule mechanics of R403Q cardiac myosin isolated from the mouse model of familial hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategy

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457-470

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4566865

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10.1093/CVR/CVV023

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4

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105

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Jolanda van der Velden

Houman Ashrafian

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2015-04-01T00:00:00Z

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271592394

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25634554

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