Ruiz-Ortega Marta, Rupérez Mónica, Esteban Vanesa, Rodríguez-Vita Juan, Sánchez-López Elsa, Carvajal Giselle, Egido Jesús
Vascular and Renal Research Laboratory, Fundación Jiménez Díaz, Avda. Reyes Católicos, 2, 28040 Madrid, Spain.
Nephrol Dial Transplant. 2006 Jan;21(1):16-20. doi: 10.1093/ndt/gfi265. Epub 2005 Nov 9.
Angiotensin II (AngII) participates in the pathogenesis of renal diseases, through the regulation of two key processes inflammation and fibrosis. AT1 and AT2 are the main receptors of AngII. AT1 mediates most of the actions of AngII. This receptor regulates the expression of profibrotic factors, such as connective tissue growth factor (CTGF). The Smad signalling pathway and the Rho/Rho kinase system are two novel mechanisms involved in AngII-induced matrix regulation recently described. The role of AT2 receptors in renal pathophysiological processes is not fully elucidated. Experimental data suggest that AT2 receptors through activation of nuclear factor-kappaB participate in renal inflammatory cell recruitment. Studies in animal models of kidney injury have shown that the combined blockade of both AT1 and AT2 receptors, as well as the inhibition of the NF-kappaB pathway are necessary to stop the inflammatory process fully. On the whole, these data highlight the complex signalling systems activated by AngII and suggest novel potential targets to block fibrosis and inflammation in renal diseases.
血管紧张素II（AngII）通过调节炎症和纤维化这两个关键过程参与肾脏疾病的发病机制。AT1和AT2是AngII的主要受体。AT1介导了AngII的大部分作用。该受体调节促纤维化因子的表达，如结缔组织生长因子（CTGF）。Smad信号通路和Rho/Rho激酶系统是最近描述的参与AngII诱导的基质调节的两种新机制。AT2受体在肾脏病理生理过程中的作用尚未完全阐明。实验数据表明，AT2受体通过激活核因子-κB参与肾脏炎症细胞募集。在肾脏损伤动物模型中的研究表明，同时阻断AT1和AT2受体以及抑制NF-κB途径对于完全阻止炎症过程是必要的。总体而言，这些数据突出了由AngII激活的复杂信号系统，并提示了阻断肾脏疾病中纤维化和炎症的新潜在靶点。
