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NDT Advance Access published online on November 9, 2005
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfi265
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Editorial Comment

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

Marta Ruiz-Ortega 1*, Mónica Rupérez 1, Vanesa Esteban 1, Juan Rodríguez-Vita 1, Elsa Sánchez-López 1, Giselle Carvajal 1, and Jesús Egido 1

1 Vascular and Renal Research Laboratory, Fundación Jiménez Diaz, Universidad Autónoma Madrid, Spain

* To whom correspondence should be addressed.
Marta Ruiz-Ortega, E-mail: mruizo{at}fjd.es



  Abstract

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-{kappa}B 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-{kappa}B 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; angiotensin-converting enzyme inhibitors; angiotensin II receptor antagonist; fibrosis; inflammation; proinflammatory cytokines; growth factors; TGF-{beta}.
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