Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction. - Wikidata - wikimedia - TriplyDB

Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.

Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.

http://www.wikidata.org/entity/Q34509413

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Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling Ablation of sarcolipin enhances sarcoplasmic reticulum calcium transport and atrial contractility Selenium and its supplementation in cardiovascular disease--what do we know?Threonine-5 at the N-terminus can modulate sarcolipin function in cardiac myocytes.Role of inotropic agents in the treatment of heart failure.Thyroid Hormone-Regulated Cardiac microRNAs are Predicted to Suppress Pathological Hypertrophic Signaling.Acquisition of a quantitative, stoichiometrically conserved ratiometric marker of maturation status in stem cell-derived cardiac myocytes.Thyroid and the heart Thyroid hormone signaling in energy homeostasis and energy metabolism.Decreased cardiac SERCA2 expression, SR Ca uptake, and contractile function in hypothyroidism are attenuated in SERCA2 overexpressing transgenic rats.Absence of myocardial thyroid hormone inactivating deiodinase results in restrictive cardiomyopathy in mice Short term triiodo-L-thyronine treatment inhibits cardiac myocyte apoptosis in border area after myocardial infarction in rats.MicroRNA 214 Is a Potential Regulator of Thyroid Hormone Levels in the Mouse Heart Following Myocardial Infarction, by Targeting the Thyroid-Hormone-Inactivating Enzyme Deiodinase Type III Differential expression of sarcolipin protein during muscle development and cardiac pathophysiology Cardiomyocyte-specific inactivation of thyroid hormone in pathologic ventricular hypertrophy: an adaptative response or part of the problem?Cardiac hypertrophy and thyroid hormone signaling American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Essential role of TEA domain transcription factors in the negative regulation of the MYH 7 gene by thyroid hormone and its receptors.New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?Restoration of thyroid hormone balance: a game changer in the treatment of heart failure?Role of thyroid hormones in ventricular remodeling.Comparative proteomics profiling of a phospholamban mutant mouse model of dilated cardiomyopathy reveals progressive intracellular stress responses.Cardiac Thyroid Hormone Metabolism and Heart Failure.Heart selenoproteins status of metabolic syndrome-exposed pups: A potential target for attenuating cardiac damage.Thyroid hormone and cardiac disease: from basic concepts to clinical application.Selenoproteins and cardiovascular stress.Myocardial Inactivation of Thyroid Hormones in Patients with Aortic Stenosis.Myocardial Induction of Type 3 Deiodinase in Dilated Cardiomyopathy.Angiotensin II does not influence expression of sarcoplasmic reticulum Ca2 + ATPase in atrial myocytes.

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Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.

http://www.wikidata.org/entity/Q34509413

description

2006 nî lūn-bûn

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2006 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2006 թվականի ապրիլին հրատարակված գիտական հոդված

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2006年の論文

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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PNAS.0601072103

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Proceedings of the National Academy of Sciences of the United States of America

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Cardiac-specific elevations in ...... d-induced cardiac dysfunction.

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Alan D Wickenden

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Anthony O Gramolini

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Benoit-Gilles Kerfant

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David H Maclennan

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Donald St Germain

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Gabriella Morreale de Escobar

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Gavin Y Oudit

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Hui Sun

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Maria Giovanna Trivieri

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Peter H Backx

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P2860

Sarcolipin inhibits polymerization of phospholamban to induce superinhibition of sarco(endo)plasmic reticulum Ca2+-ATPases (SERCAs)

Nkx2-5 pathways and congenital heart disease; loss of ventricular myocyte lineage specification leads to progressive cardiomyopathy and complete heart block

Myosin heavy chain gene expression in human heart failure

Cloning of the mammalian type II iodothyronine deiodinase. A selenoprotein differentially expressed and regulated in human and rat brain and other tissues

Sarcolipin regulates sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) by binding to transmembrane helices alone or in association with phospholamban

The molecular physiology of the cardiac transient outward potassium current (I(to)) in normal and diseased myocardium

The different cardiac expression of the type 2 iodothyronine deiodinase gene between human and rat is related to the differential response of the Dio2 genes to Nkx-2.5 and GATA-4 transcription factors

Cardiac-specific overexpression of sarcolipin inhibits sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA2a) activity and impairs cardiac function in mice

Cardiac ion channel expression and contractile function in mice with deletion of thyroid hormone receptor alpha or beta.

Thyroid hormone and the cardiovascular system.

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