摘要
脑血管病(CeVD)是造成全球死亡的主要原因之一,是全球致残的主要原因之一。脑血管病是由环境和遗传因素的相互作用引起的复杂多因素疾病。女性脑血管病发病率高于男性,直到高龄,脑血管病发生率在女性中急剧上升。因此,性别已被证实是脑血管病病因的重要危险因素,特别是缺血性卒中。尽管在类神经元损伤的机制中已经对性类固醇的重要性进行了大量研究,但实验和临床数据表明,激素并不能完全解释男性与女性的脑血管病模式。性别特异性遗传过程已经涉及动脉粥样硬化和脑血管病的不同风险风险。在这次审查中,我们讨论性别特异性脑血管病过程,描述激素对脑血管病风险的影响,转基因动物研究结果和人类遗传研究结果。此外,讨论了女性和男性缺血性卒中的遗传性以及脑血管病可能的性别特异性生物标志物的鉴定。了解脑血管病风险中激素和遗传机制之间的复杂相互作用将允许在临床实践中进行疾病治疗和预防的新的性别特异性方法
关键词: 脑血管疾病,遗传学,性别,动脉粥样硬化,激素,生物标志物
Current Medicinal Chemistry
Title:Sex-Genetic Interaction in the Risk for Cerebrovascular Disease
Volume: 24 Issue: 24
关键词: 脑血管疾病,遗传学,性别,动脉粥样硬化,激素,生物标志物
摘要: Cerebrovascular disease (CeVD) is one of the major causes of death and a leading cause of disability worldwide. CeVD is a complex and multifactorial disease caused by the interaction of environment and genetic factors. Women have lower CeVD incidence than men until an advanced age, when the incidence of CeVD rises dramatically in women. Therefore, sex has been validated as an important risk factor in the etiology of CeVD, especially ischemic stroke. Although the importance of sex steroids have been heavily studied in the mechanism of neuronal injury, the experimental and clinical data suggest that hormones do not fully account for male versus female CeVD patterns. Sex-specific genetic processes have been implicated in the different rate of risk for atherosclerosis and CeVD. In this review, we discuss sex-specific CeVD processes, describe the hormonal impact on the risk for CeVD, the results from studies in transgenic animals, and from human genetic studies. Moreover, heritability of ischemic stroke in women and men as well as identification of possible sex-specific biomarkers for CeVD are discussed. Understanding the complex interactions between hormonal and genetic mechanisms in the CeVD risk will allow for new sex-specific approaches in disease treatment and prevention in clinical practice.
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Cite this article as:
Sex-Genetic Interaction in the Risk for Cerebrovascular Disease, Current Medicinal Chemistry 2017; 24 (24) . https://dx.doi.org/10.2174/0929867324666170417100318
DOI https://dx.doi.org/10.2174/0929867324666170417100318 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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