PMID: 9525703Apr 3, 1998Paper

TGF-beta and regulation of interstitial nephritis

Mineral and Electrolyte Metabolism
Y Frishberg, C J Kelly

Abstract

TGF-beta1 has been implicated as a profibrotic growth factor in the bulk of published experimental work regarding the actions of this cytokine in kidney disease. Such investigations have spanned a methodologic spectrum from in vivo analyses to cell culture work with purified growth factors and analyses of gene expression. Important correlative work using clinical specimens has established the presence of augmented TGF-beta expression in renal diseases characterized by excessive sclerosis or fibrosis. While in the aggregate this information supports a compelling argument in favor of TGF-beta having a predominant effect to accelerate progressive renal failure, the cytokine clearly also demonstrates effects which would tend to abrogate renal injury. We provide a summary of published and new experimental data outlining immunosuppressive and 'renal-protective' actions of TGF-beta1.

Citations

Mar 11, 2000·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·K H YooR L Chevalier
Aug 28, 2001·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·B A YardF J van der Woude
Jan 5, 2002·Expert Opinion on Investigational Drugs·F Strutz
Aug 24, 1999·Current Opinion in Nephrology and Hypertension·C M Meyers
Aug 10, 2011·Nature Reviews. Nephrology·Devasmita Choudhury, Moshe Levi
Jan 6, 2001·The American Journal of Pathology·C M DuboisN G Seidah
Sep 27, 2005·Acta histochemica·Ipek AkilSevda Muftuoglu

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