Gene: environment interaction in lipid metabolism and effect on coronary heart disease risk

被引:25
|
作者
Talmud, PJ [1 ]
Humphries, SE [1 ]
机构
[1] UCL Royal Free & UCL Med Sch, British Heart Fdn Labs, London WC1E 6JJ, England
关键词
D O I
10.1097/00041433-200204000-00006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Both genetic and environmental factors influence coronary heart disease, therefore studies of coronary heart disease risk are often confounded by gene: gene and gene: environment interactions. Such interactions imply that at the molecular level there is synergy between the gene products or with the by-products of the environmental insult, resulting in a greater than additive effect on risk. Genetic risk is thus modifiable in an environment-specific manner, This review focuses on recently reported effects of smoking (environmental factor) on the impact of variation in the genes for glutathione S-transferase, paraoxonase and apolipoprotein E on the risk of coronary heart disease and effects on intermediate lipid traits. We end on a cautionary note for the need for repeat studies to confirm these reported gene: environment effects. Curr Opin Lipidol 13:149-154, (C) 2002 Lippincott Williams Wilkins.
引用
收藏
页码:149 / 154
页数:6
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