Blocking of angiotensin II is more than blocking of transforming growth factor-beta.
Fibrosis is a common feature of chronic kidney diseases that is mediated by matrix-producing myofibroblasts. One potential origin of myofibroblasts is epithelial-mesenchymal transition (EMT) of tubuloepithelial cells. Transforming growth factor-beta (TGF-beta) is a key factor inducing EMT. Carvajal et al. demonstrate that angiotensin II induces EMT by classical stimulation of TGF-beta and also by a TGF-beta-independent pathway, both signaling via Smad molecules. Therefore, blockade of angiotensin II is more than lowering of blood pressure and inhibition of TGF-beta stimulation.
Daniel
Christoph
C
Department of Nephrology and Hypertension, University of Erlangen-Nuremberg, Erlangen, Germany. Christoph.Daniel@uk-erlangen.de
D000804:Angiotensin II / Q000037:antagonists & inhibitors* / Q000502:physiology; D005355:Fibrosis; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D015398:Signal Transduction; D051785:Smad Proteins / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors* / Q000502:physiology
D051785:Smad Proteins; D016212:Transforming Growth Factor beta; D000804:Angiotensin II