leu-ser-lys-leu-peptide and Cardiomyopathies

leu-ser-lys-leu-peptide has been researched along with Cardiomyopathies* in 1 studies

Other Studies

1 other study(ies) available for leu-ser-lys-leu-peptide and Cardiomyopathies

ArticleYear
A thrombospondin-1 antagonist of transforming growth factor-beta activation blocks cardiomyopathy in rats with diabetes and elevated angiotensin II.
    The American journal of pathology, 2007, Volume: 171, Issue:3

    In diabetes and hypertension, the induction of increased transforming growth factor-beta (TGF-beta) activity due to glucose and angiotensin II is a significant factor in the development of fibrosis and organ failure. We showed previously that glucose and angiotensin II induce the latent TGF-beta activator thrombospondin-1 (TSP1). Because activation of latent TGF-beta is a major means of regulating TGF-beta, we addressed the role of TSP1-mediated TGF-beta activation in the development of diabetic cardiomyopathy exacerbated by abdominal aortic coarctation in a rat model of type 1 diabetes using a peptide antagonist of TSP1-dependent TGF-beta activation. This surgical manipulation elevates initial blood pressure and angiotensin II. The hearts of these rats had increased TSP1, collagen, and TGF-beta activity, and cardiac function was diminished. A peptide antagonist of TSP1-dependent TGF-beta activation prevented progression of cardiac fibrosis and improved cardiac function by reducing TGF-beta activity. These data suggest that TSP1 is a significant mediator of fibrotic complications of diabetes associated with stimulation of the renin-angiotensin system, and further studies to assess the blockade of TSP1-dependent TGF-beta activation as a potential antifibrotic therapeutic strategy are warranted.

    Topics: Angiotensin II; Animals; Cardiomyopathies; Diabetes Mellitus, Experimental; Fibrosis; Hemodynamics; Humans; Male; Myocardium; Peptides; Rats; Rats, Inbred WKY; Smad2 Protein; Thrombospondin 1; Transforming Growth Factor beta

2007