Document Detail


New targets for treatment of diabetic nephropathy: what we have learned from animal models.
MedLine Citation:
PMID:  23207723     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: There has been an advance in our understanding of the mechanisms of diabetic nephropathy over the past few years and much of that has occurred because of studies in animal models of diabetic nephropathy.
RECENT FINDINGS: Studies in animal models of diabetic nephropathy, especially in mice, have underlined the multifactorial nature of the pathogenesis of the disease process and the recognition that these models only partly replicate the changes found in human disease. Despite these limitations, recent animal model studies have identified a number of new, specific molecular abnormalities that point to pathways and specific molecules as potential targets for preventive or therapeutic intervention. These specific targets include the diabetic nephropathy related decreases in endothelial nitric oxide synthase activity and renal dopamine production and the increases in Nrf-2, JAK/STAT, and mammalian target of rapamycin complex 1 signaling. These and other altered signaling pathways are described in this review. We emphasize the use of a unique investigative resource, Nephromine, to utilize a library of mRNA expression data obtained from the kidney biopsies of humans with diabetic nephropathy, to compare and validate findings in mouse models with human disease.
SUMMARY: Several new pathways have been implicated in the progression of diabetic nephropathy through studies of animal models. Some of these appear to be altered in human diabetic nephropathy and may be targets for therapy.
Authors:
Frank C Brosius; Charles E Alpers
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current opinion in nephrology and hypertension     Volume:  22     ISSN:  1473-6543     ISO Abbreviation:  Curr. Opin. Nephrol. Hypertens.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-04     Completed Date:  2013-06-03     Revised Date:  2013-09-30    
Medline Journal Info:
Nlm Unique ID:  9303753     Medline TA:  Curr Opin Nephrol Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  17-25     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109-0676, USA. fbrosius@umich.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Bone Morphogenetic Proteins / metabolism
Diabetic Neuropathies / etiology,  metabolism*
Dopamine / biosynthesis
Humans
Janus Kinases / metabolism
Leptin / metabolism
NADPH Oxidase / metabolism
NF-E2-Related Factor 2 / metabolism
Nitric Oxide Synthase Type III / metabolism
Proteins / metabolism
Receptors, Leptin / metabolism
STAT Transcription Factors / metabolism
Signal Transduction*
Grant Support
ID/Acronym/Agency:
DP3 DK094311/DK/NIDDK NIH HHS; P30 DK081943/DK/NIDDK NIH HHS; P30DK081943/DK/NIDDK NIH HHS; R01 DK083391/DK/NIDDK NIH HHS; R01 DK083391/DK/NIDDK NIH HHS; R24 DK082841/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Bone Morphogenetic Proteins; 0/Leptin; 0/NF-E2-Related Factor 2; 0/Proteins; 0/Receptors, Leptin; 0/STAT Transcription Factors; 0/mechanistic target of rapamycin complex 1; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.6.3.1/NADPH Oxidase; EC 2.7.10.2/Janus Kinases
Comments/Corrections

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