Abnormalities in signaling pathways in diabetic nephropathy.
Authors Brosius FC, Khoury CC, Buller CL, Chen S
Submitted By Oliver Smithies on 3/24/2010
Status Published
Journal Expert review of endocrinology & metabolism
Year 2010
Date Published 8/1/2010
Volume : Pages 5(1) : 51 - 64
PubMed Reference 20224802
Abstract Diabetic nephropathy (DN) is characterized by a plethora of signaling
abnormalities that together ultimately result in the clinical and pathologic
hallmarks of DN, namely progressive albuminuria followed by a gradual decline in
glomerular filtration rate leading to kidney failure, and accompanied by
podocyte loss, progressive glomerular sclerosis and, ultimately, progressive
tubulointerstitial fibrosis. Over the past few years, the general understanding
of the abnormalities in signaling pathways that lead to DN has expanded
considerably. In this review, some of the important pathways that appear to be
involved in driving this process are discussed, with special emphasis on newer
findings and insights. Newer concepts regarding signaling changes in bradykinin,
mTOR, JAK/STAT, MCP-1, VEGF, endothelial nitric oxide synthase, activated
protein C and other pathways are discussed.

Investigators with authorship
Frank BrosiusUniversity of Arizona


Mcpt1mast cell protease 1
Procprotein C
Vegfavascular endothelial growth factor A
P5Ehs1protein, Chr 5, NIEHS 1
Ccl2chemokine (C-C motif) ligand 2
Mtormechanistic target of rapamycin (serine/threonine kinase)