National Institute of Cardiology, Brazilian Ministry of Health, Rio de Janeiro, Brazil.
Nutrindo Ideais Performance and Nutrition Research Center, Rio de Janeiro, Brazil.
Curr Cardiol Rev. 2023;19(4):e060223213459. doi: 10.2174/1573403X19666230206130205.
Recent evidence shows the cardiometabolic effects of estrogen administration in postmenopausal women. Women have a cardiometabolic advantage during their reproductive years, which is lost at menopause due to declining estradiol (E2). E2, also known as 17-beta-estradiol, has diverse effects in its target tissues, including the cardiovascular (CV) system, through genomic and non-genomic signaling. Metabolic changes characteristic of menopause include a worsening lipid profile, changes in body fat distribution, epicardial and pericardial fat deposition, increased susceptibility to weight gain, and increased blood pressure, resulting in an increased risk of accelerated cardiovascular disease (CVD) development. E2 mediates its cardioprotective actions by increasing mitochondrial biogenesis, angiogenesis, and vasodilation, decreasing reactive oxygen species (ROS) and oxidative stress, and modulating the renin-angiotensin-aldosterone system (RAAS). In this review, we assess whether it is prudent to develop an approach to managing postmenopausal women based on modifying the patient's CV risk that includes human-identical hormone replacement therapy (HRT), modulation of RAAS, and stimulating mitochondrial biogenesis. Further research is needed to assess the safety and benefit of HRT to reduce cardiometabolic risk.
最近的证据表明，雌激素在绝经后妇女中的心脏代谢作用。女性在生殖期具有心脏代谢优势，由于雌二醇（E2）下降，这种优势在绝经后丧失。E2，也称为 17-β-雌二醇，在其靶组织中具有多种作用，包括心血管（CV）系统，通过基因组和非基因组信号转导。绝经后的代谢变化包括血脂谱恶化、体脂分布变化、心外膜和心包脂肪沉积、体重增加易感性增加以及血压升高，从而增加加速心血管疾病（CVD）发展的风险。E2 通过增加线粒体生物发生、血管生成和血管舒张、减少活性氧（ROS）和氧化应激以及调节肾素-血管紧张素-醛固酮系统（RAAS）来介导其心脏保护作用。在这篇综述中，我们评估了是否可以明智地制定一种基于改变患者 CV 风险的方法来管理绝经后妇女，该方法包括人源化激素替代疗法（HRT）、RAAS 调节和刺激线粒体生物发生。需要进一步研究来评估 HRT 降低心脏代谢风险的安全性和益处。
