Abstract
The pathology of atherosclerotic lesions that develop in mouse models of atherosclerosis, such as those lacking apolipoprotein E or lacking the low density lipoprotein receptor, is very similar to that seen in human patients. Consequently, genetic approaches to studying atherosclerosis in these mouse models have produced a wealth of information relevant to the genetic factors and pathways that modify the early stages of atherosclerosis in humans. Despite these advances, the later stages of atherosclerosis in humans, including spontaneous plaque rupture and hemorrhage, have not been observed reliably in current mouse models. Increasing sophistication and use of genetic manipulations, however, has produced significant advances in modeling these processes. The use of genetic tools to examine the physiology, pathology, and cell biology of atherosclerosis will enhance elucidation of the pathogenesis of the disease and lead to the development of novel therapeutic strategies.
Keywords: very low density lipoproteins, quantitative trait loci, LDL receptor, atherosclerosis susceptibility, Scarb1 gene, reactive oxygen species
Current Drug Targets
Title: Genetics of Atherosclerosis in Murine Models
Volume: 8 Issue: 11
Author(s): Michael Altenburg, Jonathon Homeister, Heather Doherty and Nobuyo Maeda
Affiliation:
Keywords: very low density lipoproteins, quantitative trait loci, LDL receptor, atherosclerosis susceptibility, Scarb1 gene, reactive oxygen species
Abstract: The pathology of atherosclerotic lesions that develop in mouse models of atherosclerosis, such as those lacking apolipoprotein E or lacking the low density lipoprotein receptor, is very similar to that seen in human patients. Consequently, genetic approaches to studying atherosclerosis in these mouse models have produced a wealth of information relevant to the genetic factors and pathways that modify the early stages of atherosclerosis in humans. Despite these advances, the later stages of atherosclerosis in humans, including spontaneous plaque rupture and hemorrhage, have not been observed reliably in current mouse models. Increasing sophistication and use of genetic manipulations, however, has produced significant advances in modeling these processes. The use of genetic tools to examine the physiology, pathology, and cell biology of atherosclerosis will enhance elucidation of the pathogenesis of the disease and lead to the development of novel therapeutic strategies.
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Cite this article as:
Altenburg Michael, Homeister Jonathon, Doherty Heather and Maeda Nobuyo, Genetics of Atherosclerosis in Murine Models, Current Drug Targets 2007; 8 (11) . https://dx.doi.org/10.2174/138945007782403801
DOI https://dx.doi.org/10.2174/138945007782403801 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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