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Nephrology Dialysis Transplantation 2005 20(10):2050-2053; doi:10.1093/ndt/gfi143
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Published by Oxford University Press on behalf of ERA-EDTA [2005].

Translational Nephrology

‘As time goes by’: angiotensin II-mediated transactivation of the EGF receptor comes of age

Gunter Wolf

Department of Internal Medicine III, University of Jena, Germany

Correspondence and offprint requests to: Gunter Wolf, MD, Department of Internal Medicine III, University Hospital Jena, Erlanger Allee 101, D-07740 Jena, Germany. Email: gunter.wolf@med.uni-jena.de

The first 150 words of the full text of this article appear below.



   The renin–angiotensin system (RAS) and progression of renal disease
 
Clinical studies have provided ample evidence that inhibition of the RAS with ACE inhibitors and/or AT1-receptor blockers is an effective strategy in slowing the progression of chronic renal disease [1–3]. Although it was initially thought that inhibition of the RAS is renally protective through haemodynamic mechanisms (for example by reduction of hyperfiltration), it is now clear that angiotensin II (ANG II) is a multifactorial cytokine exhibiting growth stimulatory, proinflammatory and profibrotic effects [4–6]. These more pleiotrope effects of ANG II on the kidney were initially greeted with some skepticism [5]. At a time when the specific receptors for ANG II have only just been cloned and the ANG II-receptor blocker, saralasin, was only recently replaced with more specific agents, these reservations were not surprising [6].

ANG II binds to various receptors [6]. The AT1-subtype is involved in many . . . [Full Text of this Article]



   Relationship between ANG II and the EGF receptor
 


   A novel mechanism of ANG II-mediated transactivation of the EGF receptor
 


   Anything wrong with this landmark study?
 


   What do the novel findings mean for the practicing nephrologist?
 

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