Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress

Circulation

Volumn 105, Issue 1, 2002, Pages 85-92

  Esposito, G ^a   Rapacciuolo, A ^a   Naga Prasad, S V ^a   Takaoka, H ^a   Thomas, S A ^a   Koch, W J ^a   Rockman, H A ^a  

^a DUKE UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

Contractility; Heart failure; Hypertrophy; Receptors, adrenergic, beta; Signal transduction

Indexed keywords

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; HEART FAILURE; HEART MUSCLE CONTRACTILITY; HEART VENTRICLE HYPERTROPHY; MOUSE; NONHUMAN; PATHOPHYSIOLOGY; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; WEIGHT BEARING;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ADENYLATE CYCLASE; ANIMALS; BETA-ADRENERGIC RECEPTOR KINASE; CARDIOMEGALY; CONSTRICTION; CYCLIC AMP-DEPENDENT PROTEIN KINASES; DOPAMINE BETA-HYDROXYLASE; ECHOCARDIOGRAPHY; GTP-BINDING PROTEIN ALPHA SUBUNITS, GQ-G11; HEART; HETEROTRIMERIC GTP-BINDING PROTEINS; MICE; MICE, KNOCKOUT; MICE, TRANSGENIC; MITOGEN-ACTIVATED PROTEIN KINASES; MYOCARDIUM; ONCOGENE PROTEIN V-AKT; RECEPTORS, ADRENERGIC, BETA; RETROVIRIDAE PROTEINS, ONCOGENIC; SIGNAL TRANSDUCTION;

EID: 0036143851     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/hc0102.101365     Document Type: Article

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