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* Vanderbilt University and VA Medical Center, Nashville, Tennessee; Mount Sinai Medical School, New York, New York; University of Michigan, Ann Arbor, Michigan; Duke University and Durham VA Medical Centers, Durham, North Carolina; || Departments of Medicine and Cellular & Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; and ¶ Dorrance Hamilton Research Laboratories, Thomas Jefferson University, Philadelphia, Pennsylvania
Address correspondence to: Dr. Matthew D. Breyer, Division of Nephrology and Departments of Medicine and Molecular Physiology and Biophysics, Vanderbilt University Medical School, S3223 MCN, Division of Nephrology, Nashville, TN 37232. Phone: 615-343-9867; Fax: 615-343-4704; E-mail: matthew.breyer{at}vanderbilt.edu
Mice provide an experimental model of unparalleled flexibility for studying mammalian diseases. Inbred strains of mice exhibit substantial differences in their susceptibility to the renal complications of diabetes. Much remains to be established regarding the course of diabetic nephropathy (DN) in mice as well as defining those strains and/or mutants that are most susceptible to renal injury from diabetes. Through the use of the unique genetic reagents available in mice (including knockouts and transgenics), the validation of a mouse model reproducing human DN should significantly facilitate the understanding of the underlying genetic mechanisms that contribute to the development of DN. Establishment of an authentic mouse model of DN will undoubtedly facilitate testing of translational diagnostic and therapeutic interventions in mice before testing in humans.
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