Nephrol Dial Transplant (2003) 18: 1241-1245
© 2003 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
The thrombospondin 1–TGF-ß axis in fibrotic renal disease
Division of Nephrology, University Erlangen-Nürnberg, Erlangen, Germany
Keywords: fibrotic renal disease; TGF-ß; thrombospondin 1; thrombospondin 1–TGF-ß axis
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Introduction
Specific treatment of chronic progressive renal disease is very limited. During disease progression, extracellular matrix accumulation is the common hallmark of basically any renal process causing end-stage renal failure in man. Emerging evidence supports the concept of a major role for a thrombospondin 1 (TSP1)–TGF-ß axis in scarring renal disease.
TGF-ß is a potent cytokine affecting growth, differentiation and gene expression [1] that apparently needs to be tightly controlled. Lack of TGF-ß as demonstrated in gene-deficient mice results in a severe generalized autoinflammatory response, developmental abnormalities, increased tumorigenesis, deficient wound healing, and early death. In contrast, an excess of active TGF-ß causes enhanced tumour progression, as well as progressive fibrosis in multiple organ systems and suppression of the immune system. TGF-ß is secreted by most cell types as a latent, inactive procytokine complex that needs to be activated extracellularly to bind to its receptors [2]. Within
TGF-ß in renal disease
Thrombospondin 1 activates latent TGF-ß
Thrombospondin 1 as a potential activator of latent TGF-ß in renal cells in vitro
Thrombospondin 1 as a potential activator of latent TGF-ß in renal disease in vivo
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