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Table of Contents
Vol. 24, No. 2-3, 1998
Issue release date: March – June
Section title: Paper
Miner Electrolyte Metab 1998;24:174–180
(DOI:10.1159/000057367)

Link between Angiotensin II and TGF-β in the Kidney

Wolf G.
Department of Medicine, Division of Nephrology and Osteology, University of Hamburg, Germany

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: February 23, 1998
Issue release date: March – June

Number of Print Pages: 7
Number of Figures: 1
Number of Tables: 1

ISSN: 0378-0392 (Print)
eISSN: 1423-016X (Online)

For additional information: http://www.karger.com/MEM

Abstract

Glomerulosclerosis and tubulointerstitial fibrosis are common morphological correlates of many end-stage kidneys. There is ample evidence that transforming growth factor-β (TGF-β) plays a major role in these alterations by directly stimulating synthesis of many extracellular matrix components and reducing collagenase production, finally leading to renal scarring. Although many factors may induce TGF-β expression in the kidney, one very interesting aspect is the link between angiotensin II (ANG II) and TGF-β. Originating from observations in vascular smooth muscle cells, there are now several additional studies showing that ANG II stimulates TGF-β expression in the kidney. Although cell culture studies have convincingly demonstrated that the vasoactive peptide directly stimulates transcription as well as bioactivation of TGF-β, the in vivo evidence is more indirect. Nevertheless, there are several pathophysiological situations including unilateral ureteral obstruction, chronic cyclosporin A nephrotoxicity, various models of hypertension, and probably diabetic nephropathy in which ANG II-mediated TGF-β induction has been demonstrated to play an important role in the progression of the disease. The fascinating aspect of this relationship between ANG II and TGF-β is the fact that hemodynamic changes as well as structural changes are linked together generating a unifying model of progression of chronic renal failure with ANG II as the key player. Angiotensin-converting enzyme (ACE) inhibitor and the more recently introduced AT1-receptor blocker may be potential drugs to interfere with this ANG II-mediated TGF-β expression. Therefore, these drugs should not only be considered as antihypertensive medications, but should rather be viewed as renoprotective substances influencing renal remodeling by preventing local TGF-β expression.


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: February 23, 1998
Issue release date: March – June

Number of Print Pages: 7
Number of Figures: 1
Number of Tables: 1

ISSN: 0378-0392 (Print)
eISSN: 1423-016X (Online)

For additional information: http://www.karger.com/MEM


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