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Publication
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
Name
Institution
Frank Brosius
University of Arizona
Complications
All Complications
Bioinformatics
Bone
Cardiomyopathy
Cardiovascular
Gastro-Intestinal (GI)
Nephropathy
Neuropathy & Neurocognition
Pediatric Endocrinology
Retinopathy
Uropathy
Wound Healing
Genes
Symbol
Description
Mcpt1
mast cell protease 1
Proc
protein C
Vegfa
vascular endothelial growth factor A
P5Ehs1
protein, Chr 5, NIEHS 1
Ccl2
chemokine (C-C motif) ligand 2
Mtor
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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