PDGF-D inhibition by CR002 ameliorates tubulointerstitial fibrosis following experimental glomerulonephritis
Author(s) -
Peter Boor,
Andrzej Konieczny,
Luisa L. Villa,
Uta Kunter,
Claudia R.C. van Roeyen,
William J. LaRochelle,
Glennda Smithson,
Sharon Arrol,
Tammo Ostendorf,
Jürgen Floege
Publication year - 2007
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/gfl691
Subject(s) - medicine , platelet derived growth factor receptor , fibrosis , proteinuria , kidney , endocrinology , renal function , platelet derived growth factor , glomerulonephritis , vimentin , growth factor , immunohistochemistry , receptor
Arresting or regressing kidney scarring is of major clinical relevance. Platelet-derived growth factor D (PDGF-D) is widely expressed in fibrotic kidneys. Administration of the PDGF-D neutralizing fully human monoclonal antibody CR002 in the acute phase of progressive anti-Thy 1.1 glomerulonephritis reduced glomerular and secondary tubulointerstitial damage.
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