Endothelial Nitric Oxide Synthase Exon 7 Polymorphism, Ischemic Cerebrovascular Disease, and Carotid Atheroma | Zendy

Hugh S. Markus | Zendy; Ynte M. Ruigrok | Zendy; Nadira Ali | Zendy; John Powell | Zendy

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Endothelial Nitric Oxide Synthase Exon 7 Polymorphism, Ischemic Cerebrovascular Disease, and Carotid Atheroma

Author(s) -

Hugh S. Markus,

Ynte M. Ruigrok,

Nadira Ali,

John Powell

Publication year - 1998

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/01.str.29.9.1908

Subject(s) - medicine , odds ratio , enos , cardiology , stroke (engine) , gastroenterology , genotype , risk factor , coronary artery disease , endocrinology , nitric oxide synthase , nitric oxide , genetics , gene , mechanical engineering , engineering , biology

The role of endothelial nitric oxide synthase (eNOS) in normal physiology suggests that it could be a potential candidate gene for stroke. Reduced eNOS activity could mediate an increased stroke risk through hypertension or independent of hypertension through abnormal vasomotor responses, promoting atherogenesis, or increased platelet adhesion and aggregation. Recently, a common polymorphism in exon 7 of the eNOS gene (894G-->T) has been reported to be a strong risk factor for coronary artery disease. We determined whether it was also a risk factor for transient ischemic attack (TIA) and ischemic stroke and for carotid atheroma.

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