Oliver J A
Columbia University, Department of Medicine, New York 10032, USA.
Kidney Int. 2006 Jan;69(1):13-5. doi: 10.1038/sj.ki.5000079.
Renin can induce renal disease by generating angiotensin II and, thereby, increasing fibrosis. Huang et al describe a new mechanism of action whereby the renin-angiotensin system can also exert this effect. Direct activation of the renin/prorenin receptor in mesangial cells induced synthesis of TGF-beta and profibrotic proteins. Hence, like other proteases such as thrombin, renin and prorenin are capable of receptor-mediated cellular signaling.
肾素可通过生成血管紧张素II进而增加纤维化来诱发肾脏疾病。黄等人描述了一种新的作用机制,即肾素-血管紧张素系统也可发挥这种效应。系膜细胞中肾素/前肾素受体的直接激活可诱导转化生长因子-β和促纤维化蛋白的合成。因此,与凝血酶等其他蛋白酶一样,肾素和前肾素能够介导受体的细胞信号传导。