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Effects of TGF-beta on Podocyte Growth and Disease Progression in Proliferative Podocytopathies

Cited 33 time in Web of Science Cited 38 time in Scopus
Authors
Lee, Hyun Soon; Song, Chi Young
Issue Date
2010
Publisher
KARGER
Citation
KIDNEY & BLOOD PRESSURE RESEARCH; Vol.33 1; 24-29
Keywords
Cellular FSGSSmadsRas/ERKPodocyte TGF-betaCollapsing FSGSCrescentic glomerulonephritis
Abstract
Injured podocytes proliferate in cellular focal segmental glomerulosclerosis (FSGS), collapsing FSGS and crescentic glomerulonephritis, where TGF-beta(1) is overexpressed in hyperplastic podocytes. Yet effects of podocyte TGF-beta on podocyte growth and development of glomerulosclerosis have not been clearly defined. TGF-beta activates Smads, Ras/extracellular signal-regulated kinase (ERK) and phosphatidyl inositol-3-kinase (PI3K) pathways in podocytes, of which the major TGF-beta/Smad signaling pathway appears to override the minor TGF-beta-induced Ras/ERK/PI3K pathways. We provide evidence that increased TGF-beta/Smad signaling activity by hyperplastic podocytes may lead to mesangial cell matrix overproduction and eventually to podocyte apoptosis and/or detachment, culminating in the development of glomerulosclerosis. In this regard, TGF-beta, which is overexpressed by hyperplastic podocytes, may play an important role for the cellular and collapsing variants of FSGS to evolve into the classic FSGS pattern. In contrast, podocyte proliferation that is induced by Ras/ERK signaling activity in proliferative podocyte diseases seems to be mostly independent of TGF- beta(1) activity. Collectively, these data bring new insights into our understanding of the overexpression of TGF-beta in hyperplastic podocytes in progressive glomerular diseases. Copyright (C) 2010 S. Karger AG, Basel
ISSN
1420-4096
Language
English
URI
https://hdl.handle.net/10371/76729
DOI
https://doi.org/10.1159/000285844
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College of Medicine/School of Medicine (의과대학/대학원)Pathology (병리학전공)Journal Papers (저널논문_병리학전공)
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