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An Update on the Use of Animal Models in Diabetic Nephropathy Research

Authors
  • Betz, Boris1, 2
  • Conway, Bryan R.3
  • 1 University of Edinburgh, Centre for Inflammation Research, Edinburgh, Scotland , Edinburgh (United Kingdom)
  • 2 Jena University Hospital, Department of Clinical Chemistry and Laboratory Medicine, Jena, Germany , Jena (Germany)
  • 3 University of Edinburgh, Centre for Cardiovascular Science, Queen’s Medical Research Centre, 47 Little France Crescent, Edinburgh, EH16 4TJ, Scotland , Edinburgh (United Kingdom)
Type
Published Article
Journal
Current Diabetes Reports
Publisher
Springer-Verlag
Publication Date
Jan 27, 2016
Volume
16
Issue
2
Identifiers
DOI: 10.1007/s11892-015-0706-2
Source
Springer Nature
Keywords
License
Green

Abstract

In the current review, we discuss limitations and recent advances in animal models of diabetic nephropathy (DN). As in human disease, genetic factors may determine disease severity with the murine FVB and DBA/2J strains being more susceptible to DN than C57BL/6J mice. On the black and tan, brachyuric (BTBR) background, leptin deficient (ob/ob) mice develop many of the pathological features of human DN. Hypertension synergises with hyperglycemia to promote nephropathy in rodents. Moderately hypertensive endothelial nitric oxide synthase (eNOS−/−) deficient diabetic mice develop hyaline arteriosclerosis and nodular glomerulosclerosis and induction of renin-dependent hypertension in diabetic Cyp1a1mRen2 rats mimics moderately severe human DN. In addition, diabetic eNOS−/− mice and Cyp1a1mRen2 rats recapitulate many of the molecular pathways activated in the human diabetic kidney. However, no model exhibits all the features of human DN; therefore, researchers should consider biochemical, pathological, and transcriptomic data in selecting the most appropriate model to study their molecules and pathways of interest.

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