Bone Morphogenetic Protein 9 Reduces Cardiac Fibrosis and Improves Cardiac Function in Heart Failure

• Published in: Circulation (New York, N.Y.) Vol. 138; no. 5; pp. 513 - 526
• Main Authors: Morine, Kevin J., Qiao, Xiaoying, York, Sam, Natov, Peter S., Paruchuri, Vikram, Zhang, Yali, Aronovitz, Mark J., Karas, Richard H., Kapur, Navin K.
• Format: Journal Article
• Language: English
• Published: United States by the American College of Cardiology Foundation and the American Heart Association, Inc 31.07.2018
• Subjects: Animals; Disease Models, Animal; Endoglin - deficiency; Endoglin - genetics; Endoglin - metabolism; Fibroblasts - metabolism; Fibroblasts - pathology; Fibrosis; Growth Differentiation Factor 2 - deficiency; Growth Differentiation Factor 2 - genetics; Growth Differentiation Factor 2 - metabolism; Growth Differentiation Factors - genetics; Growth Differentiation Factors - metabolism; Haploinsufficiency; Heart Failure - genetics; Heart Failure - metabolism; Heart Failure - pathology; Heart Failure - physiopathology; Humans; Mice, Inbred C57BL; Mice, Knockout; Myocardium - metabolism; Myocardium - pathology; Phosphorylation; Recovery of Function; Signal Transduction; Smad1 Protein - metabolism; Smad3 Protein - metabolism; Ventricular Function, Left; Ventricular Remodeling; heart failure; fibrosis; endoglin; transforming growth factor beta; growth differentiation factor 2

BACKGROUND—Heart failure is a growing cause of morbidity and mortality worldwide. Transforming growth factor beta (TGF-β1) promotes cardiac fibrosis, but also activates counter-regulatory pathways that serve to regulate TGF-β1 activity in heart failure. Bone morphogenetic protein 9 (BMP9) is a membe...