Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy - sprookjes - yvandenbroek - TriplyDB

Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy

Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy

http://www.wikidata.org/entity/Q28570951

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Suppression of canonical Wnt/beta-catenin signaling by nuclear plakoglobin recapitulates phenotype of arrhythmogenic right ventricular cardiomyopathy Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5 Hypertrophic cardiomyopathy in childhood Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension Lysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophy LMNA E82K mutation activates FAS and mitochondrial pathways of apoptosis in heart tissue specific transgenic mice CMR findings in patients with hypertrophic cardiomyopathy and atrial fibrillation.Intramyocardial fibroblast myocyte communication.Angiotensin II-activated protein kinase D mediates acute aldosterone secretion.Role of Nongenomic Signaling Pathways Activated by Aldosterone During Cardiac Reperfusion Injury.Desensitization of myofilaments to Ca2+ as a therapeutic target for hypertrophic cardiomyopathy with mutations in thin filament proteins.Rescue of familial cardiomyopathies by modifications at the level of sarcomere and Ca2+ fluxes.Prevention of cardiac hypertrophy by atorvastatin in a transgenic rabbit model of human hypertrophic cardiomyopathy.Hypertrophic cardiomyopathy: from genetics to treatment Experimental therapies in hypertrophic cardiomyopathy Identification and confirmation of haptoglobin as a potential serum biomarker in hypertrophic cardiomyopathy using proteomic approaches.Molecular biology of heart disease.Genetics and clinical destiny: improving care in hypertrophic cardiomyopathy Hypertrophic cardiomyopathy: a review Genomic and nongenomic effects of aldosterone in the rat heart: why is spironolactone cardioprotective?Neuronal nitric oxide synthase inhibition improves diastolic function and reduces oxidative stress in ovariectomized mRen2.Lewis rats Myocardial late gadolinium enhancement cardiovascular magnetic resonance in hypertrophic cardiomyopathy caused by mutations in troponin I.Acute and subchronic exposure to air particulate matter induces expression of angiotensin and bradykinin-related genes in the lungs and heart: Angiotensin-II type-I receptor as a molecular target of particulate matter exposure.Protein kinase D signaling.Relationship between Regional Fat Distribution and Hypertrophic Cardiomyopathy Phenotype Genetic manipulation of 11beta-hydroxysteroid dehydrogenases in mice.Genes, calcium and modifying factors in hypertrophic cardiomyopathy.Phosphorylation of histone deacetylase 7 by protein kinase D mediates T cell receptor-induced Nur77 expression and apoptosis.Pathogenesis of hypertrophic cardiomyopathy caused by myozenin 2 mutations is independent of calcineurin activity Aldosterone and cardiovascular disease: the heart of the matter.Why are mineralocorticoid receptor antagonists cardioprotective?Genetic basis of hypertrophic cardiomyopathy.Derepression of pathological cardiac genes by members of the CaM kinase superfamily.FAT10 protects cardiac myocytes against apoptosis.Identifying genes for coronary artery disease: An idea whose time has come.Contemporary treatment of hypertrophic cardiomyopathy Aldosterone Upregulates Transient Receptor Potential Melastatin 7 (TRPM7).WIF1 causes dysfunction of heart in transgenic mice.Biomarkers of pathophysiology in hypertrophic cardiomyopathy: implications for clinical management and prognosis.Genetic fate mapping identifies second heart field progenitor cells as a source of adipocytes in arrhythmogenic right ventricular cardiomyopathy.

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Aldosterone, through novel signaling proteins, is a fundamental molecular bridge between the genetic defect and the cardiac phenotype of hypertrophic cardiomyopathy

http://www.wikidata.org/entity/Q28570951

description

2004 թուականի Մարտին հրատարակուած գիտական յօդուած

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2004 թվականի մարտին հրատարակված գիտական հոդված

@hy

artículu científicu espublizáu en 2004

@ast

im März 2004 veröffentlichter wissenschaftlicher Artikel

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scientific journal article

@en

vedecký článok (publikovaný 2004/03/16)

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vědecký článek publikovaný v roce 2004

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wetenschappelijk artikel (gepubliceerd op 2004/03/16)

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наукова стаття, опублікована в березні 2004

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مقالة علمية (نشرت في 16-3-2004)

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name

Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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type

label

Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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Aldosterone, through novel sig ...... of hypertrophic cardiomyopathy

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A. J. Marian

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Blase A. Carabello

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Gilberto DeFreitas

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Lianfeng Zhang

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Mark Entman

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Natalia Tsybouleva

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Rajnikant Patel

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Robert Roberts

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Shintaro Nemoto

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

Silvia Lutucuta

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P2860

Calmodulin-dependent kinase I regulates adrenal cell expression of aldosterone synthase

Mutations in the genes for cardiac troponin T and alpha-tropomyosin in hypertrophic cardiomyopathy

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

Reversal of cardiac and renal fibrosis by pirfenidone and spironolactone in streptozotocin-diabetic rats

The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators

Cardiac troponin T mutations result in allele-specific phenotypes in a mouse model for hypertrophic cardiomyopathy

12-lipoxygenase pathway increases aldosterone production, 3',5'-cyclic adenosine monophosphate response element-binding protein phosphorylation, and p38 mitogen-activated protein kinase activation in H295R human adrenocortical cells.

Dominant-negative effect of a mutant cardiac troponin T on cardiac structure and function in transgenic mice.

Control of CYP11B2 gene expression through differential regulation of its promoter by atypical and conventional protein kinase C isoforms.

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10

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