Reversal of fortune: estrogen receptor-β in endometriosis.

Abstract:

:Enhanced inflammation and reduced apoptosis sustain the growth of endometriotic lesions. Alterations in the expression of estrogen receptor-alpha (ERα) and estrogen receptor-beta (ERβ) accompany the conversion of resident endometrial cells within the normal uterine environment to ectopic lesions located in extrauterine 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 nongenomic 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.

journal_name

J Mol Endocrinol

authors

Simmen RC,Kelley AS

doi

10.1530/JME-16-0080

subject

Has Abstract

pub_date

2016-08-01 00:00:00

pages

F23-7

issue

2

eissn

0952-5041

issn

1479-6813

pii

JME-16-0080

journal_volume

57

pub_type

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