Journal Article

Angiotensin II: a key factor in the inflammatory and fibrotic response in kidney diseases

Marta Ruiz-Ortega, Mónica Rupérez, Vanesa Esteban, Juan Rodríguez-Vita, Elsa Sánchez-López, Giselle Carvajal and Jesús Egido

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 21, issue 1, pages 16-20
Published in print January 2006 | ISSN: 0931-0509
Published online November 2005 | e-ISSN: 1460-2385 | DOI:
Angiotensin II: a key factor in the inflammatory and fibrotic response in kidney diseases

Show Summary Details


Angiotensin II (AngII) participates in the pathogenesis of renal diseases, through the regulation of two key processes inflammation and fibrosis. AT1 and AT2 are the main receptors of AngII. AT1 mediates most of the actions of AngII. This receptor regulates the expression of profibrotic factors, such as connective tissue growth factor (CTGF). The Smad signalling pathway and the Rho/Rho kinase system are two novel mechanisms involved in AngII-induced matrix regulation recently described. The role of AT2 receptors in renal pathophysiological processes is not fully elucidated. Experimental data suggest that AT2 receptors through activation of nuclear factor-κB participate in renal inflammatory cell recruitment. Studies in animal models of kidney injury have shown that the combined blockade of both AT1 and AT2 receptors, as well as the inhibition of the NF-κB pathway are necessary to stop the inflammatory process fully. On the whole, these data highlight the complex signalling systems activated by AngII and suggest novel potential targets to block fibrosis and inflammation in renal diseases.

Keywords: angiotensin II; fibrosis; inflammation; proinflammatory cytokines; growth factors

Journal Article.  2286 words.  Illustrated.

Subjects: Nephrology

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.