The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and inflammation in a mouse model of type 1 diabetes

The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and... Diabetologia (2017) 60:1813–1821 DOI 10.1007/s00125-017-4322-3 ARTICLE The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and inflammation in a mouse model of type 1 diabetes 1 1 1 2 Pascal Bus & Marion Scharpfenecker & Priscilla Van Der Wilk & Ron Wolterbeek & 1 1 Jan A. Bruijn & Hans J. Baelde Received: 15 February 2017 /Accepted: 9 May 2017 /Published online: 15 June 2017 The Author(s) 2017. This article is an open access publication Abstract control mice (n = 5); non-diabetic control mice transfected Aims/hypothesis Animal models of diabetic nephropathy with sFlt-1(n = 10); and non-transfected diabetic mice show increased levels of glomerular vascular endothelial (n = 6). These mice were euthanised at the end of week 15. growth factor (VEGF)-A, and several studies have shown that Transfection with sFlt-1 was performed in week 6. inhibiting VEGF-A in animal models of diabetes can prevent Results We found that transfection with sFlt-1 significantly albuminuria and glomerular hypertrophy. However, in those reduced kidney damage by normalising albuminuria, glomer- studies, treatment was initiated before the onset of kidney ular hypertrophy and mesangial matrix content (i.e. glomeru- damage. Therefore, the aim of this study was to investigate lar collagen type http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Diabetologia Springer Journals

The VEGF-A inhibitor sFLT-1 improves renal function by reducing endothelial activation and inflammation in a mouse model of type 1 diabetes

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by The Author(s)
Subject
Medicine & Public Health; Internal Medicine; Metabolic Diseases; Human Physiology
ISSN
0012-186X
eISSN
1432-0428
D.O.I.
10.1007/s00125-017-4322-3
Publisher site
See Article on Publisher Site

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