Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart. - Wikidata - wikimedia - TriplyDB

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

http://www.wikidata.org/entity/Q37794503

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Transient receptor potential (TRP) channels and cardiac fibrosis MicroRNAs in Valvular Heart Diseases: Potential Role as Markers and Actors of Valvular and Cardiac Remodeling Antifibrotic therapies to control cardiac fibrosis MicroRNAs in heart failure: Small molecules with major impact Diastolic filling vortex forces and cardiac adaptations: probing the epigenetic nexus Assessment of Myocardial Fibrosis in Mice Using a T2*-Weighted 3D Radial Magnetic Resonance Imaging Sequence The fibrosis-cell death axis in heart failure Osteopontin: At the cross-roads of myocyte survival and myocardial function Thrombospondin-4 regulates fibrosis and remodeling of the myocardium in response to pressure overload Collagen XIV is important for growth and structural integrity of the myocardium Anti-remodeling effects of rapamycin in experimental heart failure: dose response and interaction with angiotensin receptor blockade MiR-133a regulates collagen 1A1: potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension Pathophysiology of Aortic Valve Stenosis: Is It Both Fibrocalcific and Sex Specific?Phenotypic screen quantifying differential regulation of cardiac myocyte hypertrophy identifies CITED4 regulation of myocyte elongation.Increased afterload induces pathological cardiac hypertrophy: a new in vitro model Cellular mechanisms of tissue fibrosis. 6. Purinergic signaling and response in fibroblasts and tissue fibrosis miR-21 is associated with fibrosis and right ventricular failure Integrins αvβ5 and αvβ3 promote latent TGF-β1 activation by human cardiac fibroblast contraction The Genetic Challenges and Opportunities in Advanced Heart Failure The calcium release-activated calcium channel Orai1 represents a crucial component in hypertrophic compensation and the development of dilated cardiomyopathy.Sphingosine 1-Phosphate Receptors: Do They Have a Therapeutic Potential in Cardiac Fibrosis?Effects of interleukin-33 on cardiac fibroblast gene expression and activity.Guanylyl cyclase (GC)-A and GC-B activities in ventricles and cardiomyocytes from failed and non-failed human hearts: GC-A is inactive in the failed cardiomyocyte.Global microRNA profiles and signaling pathways in the development of cardiac hypertrophy Discrete microstructural cues for the attenuation of fibrosis following myocardial infarction.Roles of cGMP-dependent protein kinase I (cGKI) and PDE5 in the regulation of Ang II-induced cardiac hypertrophy and fibrosis.Repression of cardiac hypertrophy by KLF15: underlying mechanisms and therapeutic implications.Augmented cardiac hypertrophy in response to pressure overload in mice lacking ELTD1.Obesity and atrial fibrillation.Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling Enhanced sensitivity to low dose irradiation of ApoE-/- mice mediated by early pro-inflammatory profile and delayed activation of the TGFβ1 cascade involved in fibrogenesis.Cardiac steatosis potentiates angiotensin II effects in the heart.The complex regulation of tanshinone IIA in rats with hypertension-induced left ventricular hypertrophy Cardiomyocyte-specific miRNA-30c over-expression causes dilated cardiomyopathy.Effects of miRNA-455 on cardiac hypertrophy induced by pressure overload.Left ventricular systolic dysfunction in asymptomatic Marfan syndrome patients is related to the severity of gene mutation: insights from the novel three dimensional speckle tracking echocardiography.Signal regulatory protein-α protects against cardiac hypertrophy via the disruption of toll-like receptor 4 signaling A microrna screen to identify regulators of peritoneal fibrosis in a rat model of peritoneal dialysis.Transforming growth factor-β inhibits myocardial PPARγ expression in pressure overload-induced cardiac fibrosis and remodeling in mice Pressure overload-dependent membrane type 1-matrix metalloproteinase induction: relationship to LV remodeling and fibrosis.

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Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

http://www.wikidata.org/entity/Q37794503

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 28 September 2010

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

@en

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

@nl

type

label

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

@en

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

@nl

prefLabel

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

@en

Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

@nl

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Cardiovascular Research

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Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

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Esther E Creemers

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Yigal M Pinto

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P2860

Serotonin and angiotensin receptors in cardiac fibroblasts coregulate adrenergic-dependent cardiac hypertrophy

Connective tissue growth factor coordinates chondrogenesis and angiogenesis during skeletal development

Regulation of cardiac gene expression by KLF15, a repressor of myocardin activity

MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue

The Kruppel-like factor KLF15 inhibits connective tissue growth factor (CTGF) expression in cardiac fibroblasts

A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure

Smads bind directly to the Jun family of AP-1 transcription factors

ATF-2 is a common nuclear target of Smad and TAK1 pathways in transforming growth factor-beta signaling

Sp1 and Smad proteins cooperate to mediate transforming growth factor-beta 1-induced alpha 2(I) collagen expression in human glomerular mesangial cells

Downregulation of miR-133 and miR-590 contributes to nicotine-induced atrial remodelling in canines

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265-272

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scholarly article

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10.1093/CVR/CVQ308

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2

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89

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2010-09-28T00:00:00Z

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20880837

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