Attenuated development of cardiac fibrosis in left ventricular pressure overload by SM16, an orally active inhibitor of ALK5

Abstract Pressure overload-induced TGF-β signaling activates cardiac fibroblasts (CFB) and leads to increased extracellular matrix (ECM) protein synthesis including fibrosis. Excessive ECM accumulation may in turn affect cardiac function contributing to development of heart failure. The aim of this...

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Veröffentlicht in:	Journal of molecular and cellular cardiology 2014-11, Vol.76, p.148-157
Hauptverfasser:	Engebretsen, Kristin V.T, Skårdal, Kristine, Bjørnstad, Sigrid, Marstein, Henriette S, Skrbic, Biljana, Sjaastad, Ivar, Christensen, Geir, Bjørnstad, Johannes L, Tønnessen, Theis
Format:	Artikel
Sprache:	eng
Schlagworte:	Administration, Oral Animals Aortic Valve Stenosis - metabolism Aortic Valve Stenosis - physiopathology Azabicyclo Compounds - administration & dosage Cardiac fibroblasts Cardiac fibrosis Cardiotonic Agents - administration & dosage Cardiovascular Cells, Cultured Collagen - metabolism Drug Evaluation, Preclinical Extracellular Matrix - metabolism Fibroblasts - drug effects Fibroblasts - metabolism Fibrosis Glycoproteins Heart failure HEK293 Cells Humans Hypertrophy, Left Ventricular - metabolism Hypertrophy, Left Ventricular - physiopathology Mice, Inbred C57BL Myocardium - pathology Pressure overload Primary Cell Culture Protein Processing, Post-Translational Protein-Serine-Threonine Kinases - antagonists & inhibitors Receptors, Transforming Growth Factor beta - antagonists & inhibitors Signal Transduction Smad2 Protein - metabolism Transforming Growth Factor beta - physiology Ventricular Pressure
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