Reviews |
From the Division of Endocrinology, Diabetes, and Hypertension (W.H.), and Department of Medicine, Division of Cardiology (R.C.D.), The David Geffen School of Medicine, University of California, Los Angeles; Division of Endocrinology, Metabolism, and Diabetes (E.D.A. and D.A.M.) and Program in Human Molecular Biology and Genetics (E.D.A.), University of Utah, Salt Lake City; Laboratory of Biochemical Genetics and Metabolism (J.L.B.), The Rockefeller University, New York; Department of Pathology and Laboratory Medicine (N.M.), University of North Carolina, Chapel Hill; Department of Medicine (E.A.F.), The Marc and Ruti Bell Program in Vascular Biology, The Leon H. Charney Division of Cardiology, New York University School of Medicine; Department of Medicine (H.D., I.J.G.), Columbia University, New York; Center for Biotechnology and Genomic Medicine (R.M.), Medical College of Georgia, Augusta; and Division of Heart and Vascular Diseases (M.K.W., C.R.-D.), National Heart, Lung, and Blood Institute, Bethesda, Md.
Correspondence to Ira J. Goldberg, Department of Medicine, Columbia University, 630 West 168th St, PH10305, New York, NY 10032. E-mail ijg3{at}columbia.edu
This Review is part of a thematic series on the Atherosclerosis in Diabetes: Dyslipidemia Versus Hyperglycemia, which includes the following articles: Do Glucose and Lipids Exert Independent Effects on Atherosclerotic Lesion Initiation or Progression to Advanced Plaques?
Recipes for Creating Animal Models of Diabetic Cardiovascular Disease
The Macrophage at the Crossroads of Insulin Resistance and Atherosclerosis Lipids, Glucose, and Oxidative Reactions in Diabetes and Atherosclerosis
Karin E. Bornfeldt Guest Editor
For more than 50 years, investigators have unsuccessfully tried to recreate in experimental animals the cardiovascular complications of diabetes seen in humans. In particular, accelerated atherosclerosis and dilated cardiomyopathy, the major causes of mortality in patients with diabetes, have been conspicuously absent in many mouse models of the disease. Under the auspices of the NIH, the Animal Models of Diabetic Complications Consortium has worked to address this issue. This effort has focused on the development of mouse models because of the high level of genomic information available and the many well-developed genetic manipulations that may be performed in mice. Importantly, the consortium has also worked to standardize many methods to assess metabolic and cardiovascular end points for measurement of the diabetic state and its macrovascular complications. Finally, for maximum benefits from these animal models in the study of atherosclerosis and of other diabetic complications, the consortium has created a system for sharing both the animal models and the accumulated phenotypic data with the greater scientific community.
Key Words: atherosclerosis diabetes mellitus diabetic cardiomyopathy transgenic mice
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