JAK/STAT signaling in renal diseases

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JAK/STAT signaling in renal diseases Peter Y. Chuang, John C. He Kidney International Volume 78, Issue 3, Pages 231-234 (August 2010) DOI: 10.1038/ki.2010.158 Copyright © 2010 International Society of Nephrology Terms and Conditions

Figure 1 Activation of JAK/STAT pathway in renal and nonrenal cells of kidney diseases. In diabetic nephropathy (DN), angiotensin II (Ang II) binding to angiotensin 1 receptor (AT1) activates JAK2/STAT1 and STAT3 in mesangial cells. In the unilateral ureteral obstruction (UUO) model of renal fibrosis, STAT3 activation has been observed in tubulointerstitial cells, which are thought to be myofibroblasts, as well as tubular epithelial cells and macrophages. In HIV-associated nephropathy (HIVAN), nef-induced podocyte proliferation occurs through Src-dependent STAT3 activation. In HgCl2-induced acute kidney injury and anti-Thy1.1 glomerulonephritis (Thy1.1 GN), STAT3 is activated in tubular epithelial cells and mesangial cells, respectively. Kidney International 2010 78, 231-234DOI: (10.1038/ki.2010.158) Copyright © 2010 International Society of Nephrology Terms and Conditions