Ablation of biglycan attenuates cardiac hypertrophy and fibrosis after left ventricular pressure overload

Journal of Molecular and Cellular Cardiology

Volumn 101, Issue , 2016, Pages 145-155

  Beetz, Nadine ^a   Rommel, Carolin ^a,b   Schnick, Tilman ^a,b   Neumann, Elena ^a,b   Lother, Achim ^a   Monroy Ordonez, Elsa Beatriz ^a   Zeeb, Martin ^a   Preissl, Sebastian ^a   Gilsbach, Ralf ^a   Melchior Becker, Ariane ^c   Rylski, Bartosz ^b   Stoll, Monika ^d   Schaefer, Liliana ^e   Beyersdorf, Friedhelm ^b   Stiller, Brigitte ^b   Hein, Lutz ^a,b  

^a UNIVERSITY OF FREIBURG   (Germany)

^b UNIVERSITY OF FREIBURG   (Germany)

^c HEINRICH HEINE UNIVERSITY   (Germany)

^d UNIVERSITY OF MÜNSTER   (Germany)

^e GOETHE UNIVERSITY   (Germany)

Author keywords

Biglycan; Cardiac hypertrophy; Heart failure; Proteoglycan

Indexed keywords

BIGLYCAN; PROTEOME;

ABRA GENE; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CARDIAC MUSCLE CELL; CELL SELECTION; CONTROLLED STUDY; FEMALE; GENE; GENE FUNCTION; GENE IDENTIFICATION; HEART LEFT VENTRICLE OVERLOAD; HEART MUSCLE CONTRACTILITY; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; IN VITRO STUDY; IN VIVO STUDY; MALE; MOLECULAR PATHOLOGY; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DETERMINATION; PROTEIN EXPRESSION; PROTEIN FUNCTION; RAT; RCAN1 GENE; SIGNAL TRANSDUCTION; TNFRSF12A GENE; UPREGULATION; ANIMAL; CARDIOMEGALY; DEFICIENCY; DISEASE MODEL; ECHOCARDIOGRAPHY; FIBROSIS; HEART LEFT VENTRICLE FUNCTION; HEART VENTRICLE REMODELING; HYPERTROPHY, LEFT VENTRICULAR; KNOCKOUT MOUSE; METABOLISM; PATHOPHYSIOLOGY; PROTEOMICS;

ANIMALS; BIGLYCAN; CARDIOMEGALY; DISEASE MODELS, ANIMAL; ECHOCARDIOGRAPHY; FEMALE; FIBROSIS; HYPERTROPHY, LEFT VENTRICULAR; MALE; MICE; MICE, KNOCKOUT; MYOCYTES, CARDIAC; PROTEOME; PROTEOMICS; RATS; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR REMODELING;

EID: 84997234972     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2016.10.011     Document Type: Article

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