Blocking of angiotensin II is more than blocking of transforming growth factor-beta.
editorial · Level V
Where this comes from
- Record sourced from PubMed, PMID 18709023.
- Also identified by DOI 10.1038/ki.2008.290.
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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.
Medical subject headings
- Angiotensin II
- Transforming Growth Factor beta