Estrogen signaling and cardiovascular disease.
Estrogen signaling and cardiovascular disease.
复制标题
DOI：
10.1161/circresaha.110.236687
复制
发表时间：
2011-09-02
影响因子：
20.1
通讯作者：
Murphy E
中科院分区：
文献类型：
--
作者：
Murphy E
Estrogen has pleiotropic effects on the cardiovascular system. The mechanisms by which estrogen confers these pleiotropic effects on cardiovascular function is under active investigation. Until a decade ago, all estrogen signaling was thought to occur by estrogen binding to nuclear estrogen receptors (ERα and ERβ), which bind to DNA and function as ligand activated transcription factors. Estrogen binding to the receptor alters gene expression thereby altering cell function. In 2000 estrogen was also shown to bind to nuclear estrogen receptors that are tethered to the plasma membrane resulting in acute activation of signaling kinases such as PI3K. An orphan G-protein coupled receptor, GPR30, has also been shown to bind estrogen and activate acute signaling pathways. ERβ has also been reported to be localized to the mitochondria, although this has been controversial. Thus estrogen can alter cell function by binding to several estrogen receptors. There appear to be mechanisms to localize these receptors to different cellular compartments, which results in complex signaling. This paper will review the different estrogen receptors and their signaling mechanisms, will also discuss mechanisms that might regulate estrogen receptor levels and locations, and lastly will consider cardiovascular effects of estrogen signaling.
