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Nat Rev Nephrol. 2018 Jan;14(1):48-56. doi: 10.1038/nrneph.2017.142. Epub 2017 Oct 24.

Modelling diabetic nephropathy in mice.

Author information

1
Cardiovascular and Metabolic Disorders Signature Research Program, Duke-NUS Medical School, 8 College Road, 169857 Singapore.
2
Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama, 236-0004 Japan.
3
Division of Nephrology, Department of Medicine, Duke University, and Durham VA Health Care System, 2 Genome Court, Durham, North Carolina 27710, USA.

Abstract

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease in the developed world. Accordingly, an urgent need exists for new, curative treatments as well as for biomarkers to stratify risk of DN among individuals with diabetes mellitus. A barrier to progress in these areas has been a lack of animal models that faithfully replicate the main features of human DN. Such models could be used to define the pathogenesis, identify drug targets and test new therapies. Owing to their tractability for genetic manipulation, mice are widely used to model human diseases, including DN. Questions have been raised, however, about the general utility of mouse models in human drug discovery. Standard mouse models of diabetes typically manifest only modest kidney abnormalities, whereas accelerated models, induced by superimposing genetic stressors, recapitulate key features of human DN. Incorporation of systems biology approaches and emerging data from genomics and metabolomics studies should enable further model refinement. Here, we discuss the current status of mouse models for DN, their limitations and opportunities for improvement. We emphasize that future efforts should focus on generating robust models that reproduce the major clinical and molecular phenotypes of human DN.

PMID:
29062142
DOI:
10.1038/nrneph.2017.142
[Indexed for MEDLINE]

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