Journal
CELL METABOLISM
Volume 6, Issue 3, Pages 164-179Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2007.07.001
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL077796, R01HL081162, R01HL077796, R01HL074086] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL77796, R01 HL081162, R01 HL074086, HL81162, R37 HL077796, HL74086, R01 HL074086-02, R01 HL077796] Funding Source: Medline
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Atherosclerosis is a complex disease involving genetic and environmental risk factors, acting on their own or in synergy. Within the general population, polymorphisms within genes in lipid metabolism, inflammation, and thrombogenesis are probably responsible for the wide range of susceptibility to myocardial infarction, a fatal consequence of atherosclerosis. Genetic linkage studies have been carried out in both humans and mouse models to identify these polymoirphisms. Approximately 40 quantitative trait loci for atherosclerotic disease have been found in humans, and approximately 30 in mice. Recently, genome-wide association studies have been used to identify atherosclerosis-susceptibility polymorphisms. Although discovering new atherosclerosis genes through these approaches remains challenging, the pace at which these polymorphisms are being found is accelerating due to rapidly improving bioinformatics resources and biotechnologies. The outcome of these efforts will not only unveil the molecular basis of atherosclerosis but also facilitate the discovery of drug targets and individualized medication against the disease.
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