The emergence of mouse models of atherosclerosis and their relevance to clinical research
Article first published online: 31 OCT 2003
Blackwell Science Ltd, 1997
Journal of Internal Medicine
Volume 242, Issue 2, pages 99–109, August 1997
How to Cite
Smith, J. D. and Breslow, J. L. (1997), The emergence of mouse models of atherosclerosis and their relevance to clinical research. Journal of Internal Medicine, 242: 99–109. doi: 10.1046/j.1365-2796.1997.00197.x
- Issue published online: 31 OCT 2003
- Article first published online: 31 OCT 2003
- Cited By
- mutant strains;
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.