Blocking of angiotensin II is more than blocking of transforming growth factor-β

被引：14

作者：

Daniel, Christoph ^{[1
]}

机构：

[1] Univ Erlangen Nurnberg, Dept Hypertens & Nephrol, D-91054 Erlangen, Germany

来源：

KIDNEY INTERNATIONAL | 2008年 / 74卷 / 05期

关键词：

D O I：

10.1038/ki.2008.290

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 [临床医学]; 100201 [内科学];

摘要：

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.

引用

页码：551 / 553

页数：4

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