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Citations to this article

Basic fibroblast growth factor augments podocyte injury and induces glomerulosclerosis in rats with experimental membranous nephropathy.
J Floege, … , W G Couser, K M Koch
J Floege, … , W G Couser, K M Koch
Published December 1, 1995
Citation Information: J Clin Invest. 1995;96(6):2809-2819. https://doi.org/10.1172/JCI118351.
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Research Article Article has an altmetric score of 3

Basic fibroblast growth factor augments podocyte injury and induces glomerulosclerosis in rats with experimental membranous nephropathy.

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Abstract

Podocyte injury is believed to contribute to glomerulosclerosis in membranous nephropathy. To identify the factors involved, we investigated the effects of basic fibroblast growth factor (bFGF), a cytokine produced by podocytes, on rats with membranous nephropathy (passive Heymann nephritis [PHN]). All rats received a daily i.v. bolus of 10 microg bFGF or vehicle from days 3-8 after PHN induction. In proteinuric PHN rats on day 8, bFGF injections further increased proteinuria. Podocytes of bFGF-injected PHN rats showed dramatic increases in mitoses, pseudocyst formation, foot process retraction, focal detachment from the glomerular basement membrane, and desmin expression. bFGF injections in PHN rats did not alter antibody or complement deposition or glomerular leukocyte influx. bFGF-injected PHN rats developed increased glomerulosclerosis when compared with control PHN rats. Also, bFGF induced proteinuria and podocyte damage in rats injected with 10% of the regular PHN-serum dose. None of these changes occurred in bFGF-injected normal rats, complement-depleted PHN rats or rats injected with 5% of the regular PHN serum dose. These divergent bFGF effects were explained in part by upregulated glomerular bFGF receptor expression, induced by PHN serum. Thus, bFGF can augment podocyte damage, resulting in increased glomerular protein permeability and accelerated glomerulosclerosis. This bFGF action is confined to previously injured podocytes. Release of bFGF from glomerular sources (including podocytes themselves) during injury may represent an important mechanism by which podocyte damage is enhanced or becomes self sustained.

Authors

J Floege, W Kriz, M Schulze, M Susani, D Kerjaschki, A Mooney, W G Couser, K M Koch

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Total citations by year

Year: 2023 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 1994 Total
Citations: 1 5 1 1 4 6 5 5 2 3 4 4 2 5 1 3 2 5 5 6 4 9 6 11 5 9 2 3 119
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Citations to this article in year 2012 (4)

Title and authors Publication Year
Acid sphingomyelinase gene knockout ameliorates hyperhomocysteinemic glomerular injury in mice lacking cystathionine-β-synthase
KM Boini, M Xia, JM Abais, M Xu, C Li, PL Li
PloS one 2012
Parietal Epithelial Cells and Podocytes in Glomerular Diseases
B Smeets, MJ Moeller
Seminars in Nephrology 2012
Selective phosphodiesterase-5 (PDE-5) inhibitor vardenafil ameliorates renal damage in type 1 diabetic rats by restoring cyclic 3',5' guanosine monophosphate (cGMP) level in podocytes
L Fang, T Radovits, G Szabo, MM Mozes, L Rosivall, G Kokeny
Nephrology Dialysis Transplantation 2012
Acid Sphingomyelinase Gene Knockout Ameliorates Hyperhomocysteinemic Glomerular Injury in Mice Lacking Cystathionine-β-Synthase
KM Boini, M Xia, JM Abais, M Xu, C Li, PL Li, C Chatziantoniou
PloS one 2012

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