Abstract
The genetics of atherosclerosis is complex, because many genes are involved and because the development of the disease is strongly influenced by environmental factors. Nevertheless, remarkable progress has been made in recent years through genetic analysis of human families and populations. In that way various candidate genes or candidate mutations have been identified that predispose individuals for premature atherosclerosis. Moving from strong correlations between mutations and phenotypes to proving that these factors are causative of atherosclerosis is, however, difficult to accomplish in the human system. For this purpose, mice generated by gene-targeting that carry precise changes in specific genes offer a unique approach to studying the role of discrete genetic factors in atherogenesis. It allows study not only of the effects in mice of candidate mutations found in humans, but also through genetic synthesis it allows study of the effects of various combinations of the mutations.
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© 1995 Kluwer Academic Publishers
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Maeda, N., Zhang, S.H., Reddick, R.L. (1995). HDL metabolism and atherogenesis in genetically modified mice. In: Assmann, G. (eds) HDL Deficiency and Atherosclerosis. Developments in Cardiovascular Medicine, vol 174. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-6585-3_7
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DOI: https://doi.org/10.1007/978-94-011-6585-3_7
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-011-6587-7
Online ISBN: 978-94-011-6585-3
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