INSERM U1048-I2MC, Faculté de Médecine, Université de Toulouse III et CHU de Toulouse, Toulouse, France.
Maturitas. 2011 Feb;68(2):165-73. doi: 10.1016/j.maturitas.2010.11.016. Epub 2010 Dec 16.
Estrogens, and in particular 17β-estradiol (E2), play a pivotal role in sexual development and reproduction and are also implicated in a large number of physiological processes including the cardiovascular system. Although epidemiological studies and Nurses' Health Study suggested, and all animal models of early atheroma clearly demonstrated a vasculoprotective action of both endogenous and exogenous estrogens, the Women's Health Initiative did not confirm the preventive action of estrogens against coronary heart disease (CHD). However, women who initiated hormone therapy closer to menopause tended to have reduced CHD risk compared with increased CHD risk among women more distant from menopause. Thus, it is now mandatory to try to understand the mechanisms that could have influenced the actions of estrogens at various stages of atherosclerosis and/or of life. In this current review, we will summarize our understanding of the potential cellular targets and mechanisms of the vasculoprotective actions of estrogens, as well as of the lack of action of estrogens when administered after a period of hormonal deprivation. The mechanisms of the aggravating role of progestogens such as medroxyprogesterone acetate will be considered. Finally, we will analyze the possibilities to uncouple some beneficial from other undesirable actions following the partial/selective activation of estrogen receptors.
雌激素，特别是 17β-雌二醇（E2），在性发育和生殖中起着关键作用，也与许多生理过程有关，包括心血管系统。尽管流行病学研究和护士健康研究表明，以及所有早期动脉粥样硬化的动物模型都清楚地表明内源性和外源性雌激素具有血管保护作用，但妇女健康倡议并未证实雌激素对冠心病（CHD）的预防作用。然而，与绝经后距离更远的女性相比，接近绝经时开始激素治疗的女性患冠心病的风险降低。因此，现在必须尝试了解可能影响动脉粥样硬化不同阶段和/或生命中雌激素作用的机制。在本综述中，我们将总结我们对雌激素血管保护作用的潜在细胞靶点和机制的理解，以及在激素剥夺一段时间后给予雌激素时缺乏作用的机制。将考虑孕激素（如醋酸甲羟孕酮）的促炎作用的机制。最后，我们将分析在雌激素受体部分/选择性激活后，从其他不良作用中分离出一些有益作用的可能性。
