Thrombospondin-2 Is Essential for Myocardial Matrix Integrity: Increased Expression Identifies Failure-Prone Cardiac Hypertrophy
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A thrombospondin-dependent pathway for a protective ER stress responseIntegrated genomic approaches implicate osteoglycin (Ogn) in the regulation of left ventricular massThe Role of Galectin-3 in the KidneysLysosomal integral membrane protein 2 is a novel component of the cardiac intercalated disc and vital for load-induced cardiac myocyte hypertrophyThrombospondin-4 regulates fibrosis and remodeling of the myocardium in response to pressure overloadBiologically relevant effects of mRNA amplification on gene expression profilesPhylogenomic analysis of vertebrate thrombospondins reveals fish-specific paralogues, ancestral gene relationships and a tetrapod innovation.Cardiac extracellular matrix remodeling: fibrillar collagens and Secreted Protein Acidic and Rich in Cysteine (SPARC)Expression profile of matricellular proteins in hypertrophied right ventricle of monocrotaline-induced pulmonary hypertensive rats.Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatmentImpact of thrombospondin-2 gene variations on the risk of thoracic aortic dissection in a Chinese Han population.Proteolysis of cell-surface tissue transglutaminase by matrix metalloproteinase-2 contributes to the adhesive defect and matrix abnormalities in thrombospondin-2-null fibroblasts and mice.Galectin-3 in heart failure with preserved ejection fraction. A RELAX trial substudy (Phosphodiesterase-5 Inhibition to Improve Clinical Status and Exercise Capacity in Diastolic Heart Failure).The thrombospondins.Endogenous thrombospondin 1 protects the pressure-overloaded myocardium by modulating fibroblast phenotype and matrix metabolismMatricellular proteins in cardiac adaptation and disease.Endothelial nitric oxide synthase controls the expression of the angiogenesis inhibitor thrombospondin 2Changes in the myocardial interstitium and contribution to the progression of heart failure.Evaluation of Left Ventricle Function by Regional Fractional Area Change (RFAC) in a Mouse Model of Myocardial Infarction Secondary to Valsartan Treatment.Breeding Strategy Determines Rupture Incidence in Post-Infarct Healing WARPing Cardiovascular Research.Characterization of the Transcriptional Complexity of the Receptive and Pre-receptive Endometria of Dairy GoatsLack of thrombospondin-2 reduces fibrosis and increases vascularity around cardiac cell grafts.Proangiogenic Properties of Thrombospondin-4.Extracellular matrix and fibroblast communication following myocardial infarction.Thrombospondins in the transition from myocardial infarction to heart failure.Relationship of plasma galectin-3 to renal function in patients with heart failure: effects of clinical status, pathophysiology of heart failure, and presence or absence of heart failure.Cellular mechanisms of tissue fibrosis. 2. Contributory pathways leading to myocardial fibrosis: moving beyond collagen expression.Maternal undernutrition induces differential cardiac gene expression in pulmonary hypertensive steers at high elevation.Thrombospondin-2 modulates extracellular matrix remodeling during physiological angiogenesisEndothelial progenitor cells in neovascularization of infarcted myocardiumInflammation as a therapeutic target in heart failure? A scientific statement from the Translational Research Committee of the Heart Failure Association of the European Society of Cardiology.Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodellingMacrophage fusion, giant cell formation, and the foreign body response require matrix metalloproteinase 9.Enhanced angiogenesis and reduced contraction in thrombospondin-2-null wounds is associated with increased levels of matrix metalloproteinases-2 and -9, and soluble VEGF.The pathogenesis of cardiac fibrosis.Defective peroxisomal proliferators activated receptor gamma activity due to dominant-negative mutation synergizes with hypertension to accelerate cardiac fibrosis in miceThrombospondin-2 and SPARC/osteonectin are critical regulators of bone remodeling.Thrombospondins in the heart: potential functions in cardiac remodeling.Regulation of myocardial SERCA2a expression in ventricular hypertrophy and heart failure.Cardiomyocyte-specific transforming growth factor β suppression blocks neutrophil infiltration, augments multiple cytoprotective cascades, and reduces early mortality after myocardial infarction.
P2860
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P2860
Thrombospondin-2 Is Essential for Myocardial Matrix Integrity: Increased Expression Identifies Failure-Prone Cardiac Hypertrophy
description
2004 nî lūn-bûn
@nan
2004 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
name
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@ast
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@en
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@nl
type
label
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@ast
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@en
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@nl
prefLabel
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@ast
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@en
Thrombospondin-2 Is Essential ...... lure-Prone Cardiac Hypertrophy
@nl
P2093
P3181
P1433
P1476
Thrombospondin-2 is essential ...... lure-prone cardiac hypertrophy
@en
P2093
Ben J A Janssen
Blanche Schroen
Harry J G M Crijns
J Gordon Porter
Jack P M Cleutjens
Jacques J M Debets
Jos F M Smits
Paul Bornstein
Rick E W van Leeuwen
Rudy Duisters
P304
P3181
P356
10.1161/01.RES.0000141019.20332.3E
P407
P577
2004-07-29T00:00:00Z