Genetic association between eNOS gene polymorphisms and risk of carotid atherosclerosis
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Yongheng Chen1 · Lin Chen1 · Qiliang Zhou2,3 1
Department of Cardiology, The First Affiliated Hospital, Changsha Medical University, Changsha, China Department of Human Anatomy, School of Basic Medical Science, Changsha Medical University, Changsha, China 3 Department of Human Anatomy, Histology and Embryology, Institute of Neuroscience, Changsha Medical University, Changsha, China 2
Genetic association between eNOS gene polymorphisms and risk of carotid atherosclerosis A meta-analysis
Electronic supplementary material The online version of this article (https://doi. org/10.1007/s00059-020-04995-z) contains supplementary material, which is available to authorized users.
Background Atherosclerosis is a systemic disease with systemic muscular activity and often occurs simultaneously in arteries such as the coronary artery and carotid artery [1, 2], which correspondingly causes ischemic changes in the heart and brain. The intimal thickening of vascular walls has been shown to be the early stage of atherosclerosis [3, 4]. Plaque formation is an obvious characteristic of atherosclerosis and may reflect the degree ofatherosclerosis [5]. Carotid atherosclerosis (CAS) is closely related to cerebrovascular diseases and cardiovascular diseases [6, 7]. Coronary atherosclerosis and CAS have a common pathogenesis and similar pathophysiological basis [8]. Researchers have reported that CAS and coronary atherosclerosis share a number of common risk factors such as age, sex (male), smoking, hypertension, diabetes, and low-density lipoprotein cholesterol levels [9–11]. Carotid atherosclerosis is a quantitative measure of generalized atherosclerosis, with significant predictive value for subsequent
myocardial infarction and stroke [12]. Therefore, CAS may indirectly reflect the degree and scope of coronary artery disease. Both genetic and environmental factors were shown to be associated with the development of CAS [13, 14]. In fact, a study of monozygotic twins has shown that atherosclerosis has a strong genetic component [15]. Multiple candidate genes have been reported to be associated with susceptibility to atherosclerosis as well as to CAS [16–19]. Endotheliumderived nitric oxide (NO), synthesized by the constitutively expressed endothelial nitric oxide synthetase (eNOS) in endothelial cells, platelets, and red blood cells, has been revealed to have important anti-atherogenic properties, which could inhibit platelet aggregation and adhesion [20–22]. Evidence has shown that diminished NO production may lead to endothelial dysfunction, which may contribute to atherosclerosis [23]. In addition, experiments on animal models provided evidence that mice without the eNOS gene have accelerated atherosclerosis [24]. Several polymorphisms of the eNOS gene have been identified. The polymorphisms T786C, G894T, and 4a/4b have been reported to be associated with the development of atherosclerosis. Among them, G894T was the only functional polymorphism changing the eNOS protein sequences at codon 298, and then
leading to reduced basal NO produ
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