Blocking of angiotensin II is more than blocking of transforming growth factor-beta - PubMed (original) (raw)
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doi: 10.1038/ki.2008.290.
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- PMID: 18709023
- DOI: 10.1038/ki.2008.290
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Blocking of angiotensin II is more than blocking of transforming growth factor-beta
Christoph Daniel. Kidney Int. 2008 Sep.
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Abstract
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.
Comment on
- Angiotensin II activates the Smad pathway during epithelial mesenchymal transdifferentiation.
Carvajal G, Rodríguez-Vita J, Rodrigues-Díez R, Sánchez-López E, Rupérez M, Cartier C, Esteban V, Ortiz A, Egido J, Mezzano SA, Ruiz-Ortega M. Carvajal G, et al. Kidney Int. 2008 Sep;74(5):585-95. doi: 10.1038/ki.2008.213. Epub 2008 May 28. Kidney Int. 2008. PMID: 18509316
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