| New targets for treatment of diabetic nephropathy: what we have learned from animal models. | |
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MedLine Citation:
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PMID: 23207723 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Frank C Brosius; Charles E Alpers |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Current opinion in nephrology and hypertension Volume: 22 ISSN: 1473-6543 ISO Abbreviation: Curr. Opin. Nephrol. Hypertens. Publication Date: 2013 Jan |
Date Detail:
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Created Date: 2012-12-04 Completed Date: 2013-06-03 Revised Date: 2013-06-14 |
Medline Journal Info:
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Nlm Unique ID: 9303753 Medline TA: Curr Opin Nephrol Hypertens Country: England |
Other Details:
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Languages: eng Pagination: 17-25 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109-0676, USA. fbrosius@umich.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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DP3 DK094311/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:
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0/Bone Morphogenetic Proteins; 0/Leptin; 0/NF-E2-Related Factor 2; 0/Proteins; 0/Receptors, Leptin; 0/STAT Transcription Factors; 0/mTORC1 complex, mouse; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.6.3.1/NADPH Oxidase; EC 2.7.10.2/Janus Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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