[Genes and coronary heart disease].
The causes of atherosclerotic cardiovascular disease have been intensely scrutinized for the last few decades. Since the classic risk factors have been found to be incomplete predictors of the disease, additional risk factors based on molecular genetics are now being sought. Polymorphisms are gene variations that have only modest effects on the function of coded proteins or enzymes. However, they are common and may be risk factors in the presence of environmental risk factors (cholesterol, stress, tobacco). Recent advances in molecular biology have made it possible to detect numerous polymorphisms that might have a detrimental effect on vascular biology, suggesting the hypothesis that multiple polymorphisms in the presence of environmental factors could act synergistically in the pathogenesis of atherosclerosis and coronary heart disease, which are typically polygenic and multifactorial diseases. In this review, the current status of our knowledge of polymorphisms and mutations potentially implicated in the mechanisms of coronary artery disease is discussed. Genotype/phenotype, gene-gene, and gene-environmental interactions related to lipid metabolism, the renin-angiotensin-aldosterone and adrenergic systems, insulin resistance, oxidative stress and endothelial function, inflammation and thrombosis are analyzed. Individual coronary risk might be related to the presence of a critical accumulation detrimental polymorphisms.
Navarro-López
Francisco
F
Servicio de Cardiología, Hospital Clínico (IDIBAPS), Universidad de Barcelona, Spain. navarro@mediciina.ub.es
D003327:Coronary Disease / Q000235:genetics*; D006801:Humans; D006973:Hypertension / Q000235:genetics; D007249:Inflammation / Q000235:genetics; D007333:Insulin Resistance / Q000235:genetics; D008075:Lipoproteins, HDL / Q000235:genetics; D008077:Lipoproteins, LDL / Q000235:genetics; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System; D013927:Thrombosis / Q000235:genetics
D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL