The G protein-coupled estrogen receptor GPER/GPR30 as a regulator of cardiovascular function.
The G protein-coupled estrogen receptor GPER/GPR30 as a regulator of cardiovascular function.
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G蛋白偶联的雌激素受体GPER/GPR30作为心血管功能的调节剂。
DOI：
10.1016/j.vph.2011.06.003
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发表时间：
2011-07
影响因子：
4
通讯作者：
Barton, Matthias
中科院分区：
文献类型：
--
作者：
Meyer, Matthias R.;Prossnitz, Eric R.;Barton, Matthias
内源性雌激素是绝经前妇女心血管动态平衡的重要调节因子，可干预高血压和冠心病的发生发展。这些激素通过三种不同的雌激素受体发挥作用，在复杂的相互作用中影响基因转录和快速信号通路。除了经典的雌激素受体ERα和ERβ外，最近还发现了一种在心血管系统表达的G蛋白偶联的雌激素受体，称为GPER。内源性17β-雌二醇、选择性雌激素受体调节剂(包括他莫昔芬和雷洛昔芬)以及选择性雌激素受体下调调节剂(如ICI182、780)都是GPER的激动剂，参与调节血管舒缩张力和保护心肌缺血/再灌注损伤。因此，理解ERα、ERβ和GPER在心血管功能中的单独作用变得越来越复杂。随着越来越多的证据表明GPER负责雌激素对心血管的多种有益作用，该受体可能代表着一个新的靶点，通过组织特异性的、选择性地激活雌激素依赖的分子通路来开发有效的治疗心血管疾病的策略，而这些分子通路没有传统激素疗法的副作用。
Endogenous estrogens are important regulators of cardiovascular homeostasis in premenopausal women and interfere with the development of hypertension and coronary artery disease. These hormones act via three different estrogen receptors affecting both gene transcription and rapid signaling pathways in a complex interplay. In addition to the classical estrogen receptors ERα and ERβ, which are known mediators of estrogen-dependent vascular effects, a G protein-coupled estrogen receptor termed GPER that is expressed in the cardiovascular system has recently been identified. Endogenous human 17β-estradiol, selective estrogen receptor modulators (SERMs) including tamoxifen and raloxifene, and selective estrogen receptor downregulators (SERDs) such as ICI 182,780 are all agonists of GPER, which has been implicated in the regulation of vasomotor tone and protection from myocardial ischemia/reperfusion injury. As a result, understanding the individual role of ERα, ERβ, and GPER in cardiovascular function has become increasingly complex. With accumulating evidence that GPER is responsible for a variety of beneficial cardiovascular effects of estrogens, this receptor may represent a novel target to develop effective strategies for the treatment of cardiovascular diseases by tissue-specific, selective activation of estrogen-dependent molecular pathways devoid of side effects seen with conventional hormone therapy.
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影响因子：
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作者：
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DOI：
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