Abstract:
Many studies have shown that an increase in cardiovascular disease in women is related to hormonal changes occurring particularly after menopause with increasing age. While the results of large clinical trials reporting no benefit of hormone replacement therapy (HRT) in cardiovascular disease have been known for some time, there is an increasing body of knowledge regarding the various mechanisms by which estrogen modulates platelet function that could in part explain the higher cardiovascular risk occurring in postmenopausal women and potential benefits of HRT on cardiovascular health. Our review summarizes our current knowledge regarding the effect of endogenous and exogenous estrogen on platelet activity, which can help researchers design future studies. We collected information from 21 peer-reviewed articles published from 1993 to 2021. Studies have indicated that postmenopausal women have higher platelet activity than premenopausal women, which can increase the risk of thrombo-embolic events and cardiovascular disease. Although some studies have reported pro-thrombotic effects of estrogen replacement therapy such as increased platelet activation and adhesion, other studies demonstrated decreased platelet aggregation by inhibiting GP IIb/IIIa receptor expression. This is mediated by estrogen receptors on the platelet membrane in a non-genomic manner and suggests an opportunity for the usage of estrogen replacement therapy with subtle changes in the formulation and route, particularly if started early after menopause. The effect of estrogen on platelet activity is promising as an important factor in reducing the risk of cardiovascular events, warranting further investigation.
摘要:
许多研究表明,女性心血管疾病的增加与荷尔蒙变化有关,尤其是在绝经后随着年龄的增长而发生的变化。虽然大型临床试验的结果报道激素替代疗法(HRT)在心血管疾病中没有益处已经知道了一段时间,关于雌激素调节血小板功能的各种机制的知识越来越多,这在一定程度上解释了绝经后妇女心血管风险较高以及HRT对心血管健康的潜在益处.我们的综述总结了我们目前关于内源性和外源性雌激素对血小板活性的影响的知识,这可以帮助研究人员设计未来的研究。我们从1993年至2021年发表的21篇同行评审文章中收集了信息。研究表明,绝经后妇女的血小板活性高于绝经前妇女,这会增加血栓栓塞事件和心血管疾病的风险。尽管一些研究报道了雌激素替代疗法的促血栓作用,例如增加血小板活化和粘附,其他研究表明,血小板聚集通过抑制GPIIb/IIIa受体表达而减少.这是由血小板膜上的雌激素受体以非基因组方式介导的,并暗示了使用雌激素替代疗法的机会,其配方和途径发生了细微变化,特别是在更年期后早期开始。雌激素对血小板活性的影响有望成为降低心血管事件风险的重要因素,保证进一步调查。