Glucocorticoid Receptor Gene and Coronary Artery Disease: Right Idea, Wrong Gene Variant?
نویسندگان
چکیده
منابع مشابه
Glucocorticoid receptor gene and coronary artery disease: right idea, wrong gene variant?
Artery Disease: Right Idea, Wrong Gene Variant? To the Editor: Recent data reported by Lin et al1 suggest that coronary artery disease (CAD) is associated with an Asn363Ser variant in exon 2 of the glucocorticoid receptor gene (GRL). The study is based on the notion that a dysfunctional glucocorticoid receptor may add to the adverse health effects of excessive cortisol concentrations. In a prev...
متن کاملGlucocorticoid Receptor Gene and Coronary Artery Disease: Right Idea, Wrong Gene Variant?
Artery Disease: Right Idea, Wrong Gene Variant? To the Editor: Recent data reported by Lin et al1 suggest that coronary artery disease (CAD) is associated with an Asn363Ser variant in exon 2 of the glucocorticoid receptor gene (GRL). The study is based on the notion that a dysfunctional glucocorticoid receptor may add to the adverse health effects of excessive cortisol concentrations. In a prev...
متن کاملAssociation of coronary artery disease with glucocorticoid receptor N363S variant.
Overweight is associated with the N363S variant in the glucocorticoid receptor (encoded by nuclear receptor subfamily 3, group C, member 1 gene: NR3C1). The present study examined whether the N363S polymorphism might also be associated with coronary artery disease (CAD). This involved 556 patients with CAD, of which 437 were analyzed, and 302 control subjects, all being of Anglo-Celtic descent ...
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Subject & Aim. Endothelial nitric oxide synthase (eNOS) is one of the most important candidate genes in CAD. A functional polymorphism within eNOS gene is a 27 bp VNTR on its intron 4 which has been shown to be associated with various diseases. In this study we investigated eNOS VNTR polymorphism in addition to eNOS gene expression profile in patients with CAD. Material and Methods. The study c...
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ژورنال
عنوان ژورنال: Hypertension
سال: 2003
ISSN: 0194-911X,1524-4563
DOI: 10.1161/01.hyp.0000081965.51761.aa