Feliers Denis, Kasinath Balakuntalam S
Division of Nephrology, Department of Medicine, O'Brien Kidney Research Center, University of Texas Health Science Center, San Antonio, TX 78229, USA.
J Signal Transduct. 2011;2011:768512. doi: 10.1155/2011/768512. Epub 2011 Apr 7.
Acute or chronic kidney injury results from various insults and pathological conditions, and is accompanied by activation of compensatory repair mechanisms. Both insults and repair mechanisms are initiated by circulating factors, whose cellular effects are mediated by activation selective signal transduction pathways. Two main signal transduction pathways are activated during these processes, the phosphatidylinositol 3' kinase (PI-3K)/mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase (MAPK) cascades. This review will focus on the latter, and more specifically on the role of extracellular signal-regulated kinase (ERK) cascade in kidney injury and repair.
急性或慢性肾损伤由多种损伤因素和病理状况引起,并伴有代偿性修复机制的激活。损伤因素和修复机制均由循环因子启动,这些循环因子的细胞效应通过激活选择性信号转导通路介导。在这些过程中激活了两条主要的信号转导通路,即磷脂酰肌醇3'激酶(PI-3K)/雷帕霉素哺乳动物靶蛋白(mTOR)和丝裂原活化蛋白激酶(MAPK)级联反应。本综述将聚焦于后者,更具体地说,是细胞外信号调节激酶(ERK)级联反应在肾损伤和修复中的作用。