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Abnormalities in signaling pathways in diabetic nephropathy.
Brosius FC, Khoury CC, Buller CL, Chen S
Oliver Smithies on 3/24/2010
Expert review of endocrinology & metabolism
Volume : Pages
5(1) : 51 - 64
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
University of Arizona
Neuropathy & Neurocognition
mast cell protease 1
vascular endothelial growth factor A
protein, Chr 5, NIEHS 1
chemokine (C-C motif) ligand 2
mechanistic target of rapamycin (serine/threonine kinase)
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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