The emergence of mouse models of atherosclerosis and their relevance to clinical research

The emergence of mouse models of atherosclerosis and their relevance to clinical research Smith JD, Breslow JL (Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University, New York, NY, USA). The emergence of mouse models of atherosclerosis and their relevance to clinical research (Review). J Intern Med 1997; 242: 99–109. Due to the ability to introduce or mutate genes, the mouse has become the most common experimental animal model for atherosclerosis research. Wildtype mice on a chow diet do not get atherosclerosis. Three ways to induce atherosclerosis in mice are discussed: diet‐induced, apoE deficiency‐induced, and LDL receptor‐deficiency induced. The atherosclerotic lesions in apoE‐deficient mice have been well characterized, and they resemble human lesions in their sites of predilection and progression to the fibroproliferative stage. These mouse models of atherosclerosis are being used to identify genes which modify atherosclerosis susceptibility and in the development of antiatherogenic therapies. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Internal Medicine Wiley

The emergence of mouse models of atherosclerosis and their relevance to clinical research

Journal of Internal Medicine, Volume 242 (2) – Aug 1, 1997

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Publisher
Wiley
Copyright
Blackwell Science Ltd, 1997
ISSN
0954-6820
eISSN
1365-2796
D.O.I.
10.1046/j.1365-2796.1997.00197.x
Publisher site
See Article on Publisher Site

Abstract

Smith JD, Breslow JL (Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University, New York, NY, USA). The emergence of mouse models of atherosclerosis and their relevance to clinical research (Review). J Intern Med 1997; 242: 99–109. Due to the ability to introduce or mutate genes, the mouse has become the most common experimental animal model for atherosclerosis research. Wildtype mice on a chow diet do not get atherosclerosis. Three ways to induce atherosclerosis in mice are discussed: diet‐induced, apoE deficiency‐induced, and LDL receptor‐deficiency induced. The atherosclerotic lesions in apoE‐deficient mice have been well characterized, and they resemble human lesions in their sites of predilection and progression to the fibroproliferative stage. These mouse models of atherosclerosis are being used to identify genes which modify atherosclerosis susceptibility and in the development of antiatherogenic therapies.

Journal

Journal of Internal MedicineWiley

Published: Aug 1, 1997

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