阻断血管紧张素 II 不仅仅是阻断转化生长因子-β。

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

作者信息

Daniel Christoph

机构信息

Department of Nephrology and Hypertension, University of Erlangen-Nuremberg, Erlangen, Germany.

出版信息

Kidney Int. 2008 Sep;74(5):551-3. doi: 10.1038/ki.2008.290.

DOI:10.1038/ki.2008.290

PMID:18709023

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.

摘要

纤维化是慢性肾病的一个常见特征，由产生基质的肌成纤维细胞介导。肌成纤维细胞的一个潜在来源是肾小管上皮细胞的上皮-间质转化（EMT）。转化生长因子-β（TGF-β）是诱导EMT的关键因子。卡瓦哈尔等人证明，血管紧张素II通过经典的TGF-β刺激以及通过不依赖TGF-β的途径诱导EMT，两者均通过Smad分子发出信号。因此，阻断血管紧张素II不仅仅是降低血压和抑制TGF-β刺激。