Format

Send to

Choose Destination
See comment in PubMed Commons below
Curr Opin Nephrol Hypertens. 2011 May;20(3):278-84. doi: 10.1097/MNH.0b013e3283451901.

Mouse models of diabetic nephropathy.

Author information

1
Department of Pathology, University of Washington Medical Center, Seattle, Washington 98195, USA. calp@uw.edu

Abstract

PURPOSE OF REVIEW:

Progress in identification of effective therapies for diabetic nephropathy continues to be limited by the lack of ideal animal models. Here we review the current status of some leading murine models of this disorder.

RECENT FINDINGS:

A consensus statement of the Animals Models of Diabetic Complications Consortium sets forth guidelines and standards for measuring renal function and structural parameters necessary for validating murine models of diabetic nephropathy. Two murine models exploiting endothelial nitric oxide synthase (eNOS) deficiency as a major susceptibility factor for development of diabetic nephropathy are among the very few options for studying features of advanced diabetic nephropathy. Akita and OVE26 mice with mutations that result in Type I diabetes are also useful models of diabetic nephropathy. The recently described BTBR ob/ob (leptin deficient) mouse with Type II diabetes demonstrates key features of early podocyte loss and mesangiolysis characteristic of human diabetic nephropathy.

SUMMARY:

While there are many murine models of mesangial matrix expansion in the setting of diabetes, few progress to develop advanced diabetic lesions. Mice with eNOS deficiency, OVE26 mice, and the recently described BTBR ob/ob mouse currently appear to be the best murine models of advanced disease. A model that allows testing of interventions that modulate podocyte loss and regeneration, such as the BTBR ob/ob mouse, may be of particular benefit in developing therapeutics for diabetic nephropathy.

PMID:
21422926
PMCID:
PMC3658822
DOI:
10.1097/MNH.0b013e3283451901
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer Icon for PubMed Central
    Loading ...
    Support Center