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Angiotensin II stimulates α3(IV) collagen production in mouse podocytes via TGF-β and VEGF signalling: implications for diabetic glomerulopathy
Author(s) -
Sheldon Chen,
Joseph S. Lee,
M. Carmen Iglesiasde la Cruz,
Amy Wang,
Adriana IzquierdoLahuerta,
Nisha K. Gandhi,
Farhad R. Danesh,
Günter Wolf,
Fuad N. Ziyadeh
Publication year - 2005
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfh837
Subject(s) - endocrinology , autocrine signalling , medicine , podocyte , angiotensin ii , transforming growth factor , vascular endothelial growth factor , downregulation and upregulation , transforming growth factor beta , receptor , microbiology and biotechnology , chemistry , biology , kidney , biochemistry , proteinuria , vegf receptors , gene
The podocyte is bathed in an angiotensin II (AngII)-rich ultrafiltrate, but the impact of AngII on podocyte pathobiology is not well known. Because podocytes play a direct role in the glomerular basement membrane (GBM) thickening of diabetes, the alpha3(IV) collagen chain was examined. Podocyte expression of alpha3(IV) collagen may involve the transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) systems.

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