Reversal of fortune: estrogen receptor-β in endometriosis.
Reversal of fortune: estrogen receptor-β in endometriosis.
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DOI：
10.1530/jme-16-0080
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发表时间：
2016-08
影响因子：
3.5
通讯作者：
Kelley AS
中科院分区：
文献类型：
--
作者：
Simmen RC;Kelley AS
炎症增强和细胞凋亡减少维持子宫内膜异位病变的生长。雌激素受体 (ER) α 和 β 表达的变化伴随着正常子宫环境内的常驻子宫内膜细胞向位于子宫外部位的异位病变的转变。这篇重点综述中强调的最新研究将 ERβ 与细胞凋亡和炎症网络的失调联系起来，涉及子宫内膜异位症中新的相互作用伙伴。使用人类细胞和小鼠模型阐明 ERβ 的这些非基因组作用，是了解导致疾病建立和进展的关键调控途径被破坏的重要一步。
Enhanced inflammation and reduced apoptosis sustain the growth of endometriotic lesions. Alterations in the expression of estrogen receptor (ER) α and β accompany the conversion of resident endometrial cells within the normal uterine environment to ectopic lesions located in extra-uterine sites. Recent studies highlighted in this focused review linked ERβ to dysregulation of apoptotic and inflammatory networks involving novel interacting partners in endometriosis. The elucidation of these non-genomic actions of ERβ using human cells and mouse models is an important step in understanding key regulatory pathways that are disrupted leading to disease establishment and progression.