Tenascin-C promotes chronic pressure overload-induced cardiac dysfunction, hypertrophy and myocardial fibrosis

AIMS:Left ventricular (LV) hypertrophy is characterized by cardiomyocyte hypertrophy and interstitial fibrosis ultimately leading to increased myocardial stiffness and reduced contractility. There is substantial evidence that the altered expression of matrix metalloproteinases (MMP) and Tenascin-C (...

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Veröffentlicht in:	Journal of hypertension 2018-04, Vol.36 (4), p.847-856
Hauptverfasser:	Podesser, Bruno K, Kreibich, Maximilian, Dzilic, Elda, Santer, David, Förster, Lorenz, Trojanek, Sandra, Abraham, Dietmar, Krššák, Martin, Klein, Klaus U, Tretter, Eva V, Kaun, Christoph, Wojta, Johann, Kapeller, Barbara, Gonçalves, Inês Fonseca, Trescher, Karola, Kiss, Attila
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Basigin - genetics Basigin - metabolism Cardiac Output Cell Line Fibrosis Genotype Hypertension - complications Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - metabolism Hypertrophy, Left Ventricular - physiopathology Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - metabolism Mice, Inbred C57BL Mice, Knockout Myocardium - pathology Myocytes, Cardiac - pathology Natriuretic Peptide, Brain - metabolism Signal Transduction Tenascin - genetics Tenascin - metabolism Ventricular Remodeling - genetics Ventricular Remodeling - physiology
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