Inflammatory gene polymorphisms and ischaemic heart disease: review of population association studies.
Inflammation and genetics are both prominent mechanisms in the pathogenesis of atherosclerosis and arterial thrombosis. Accordingly, a number of population studies have explored the association of ischaemic heart disease with gene polymorphisms of the inflammatory molecules tumour necrosis factors (TNF) alpha and beta, transforming growth factors (TGF) beta1 and 2, interleukin (IL) 1 and its receptor antagonist (IL 1ra), CD14 (the receptor for lipopolysaccharide), P and E selectins, and platelet endothelial cell adhesion molecule (PECAM) 1. Although they are very preliminary and partly conflicting, the data provide some evidence that alterations in the genetics of the inflammatory system may modify the risk of ischaemic heart disease.
Andreotti
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Institute of Cardiology, Catholic University, Rome, Italy. felicita.andreotti@iol.it
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Crea
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D000328:Adult; D019040:E-Selectin / Q000235:genetics; D005260:Female; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D007375:Interleukin-1 / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000235:genetics; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000235:genetics*; D019007:P-Selectin / Q000235:genetics; D010641:Phenotype; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors; D016211:Transforming Growth Factor alpha / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D019040:E-Selectin; D007375:Interleukin-1; D018950:Lipopolysaccharide Receptors; D019007:P-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D016211:Transforming Growth Factor alpha; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha