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 Endocrinoljournal_title
Journal of molecular endocrinologyauthors
Simmen RC,Kelley ASdoi
10.1530/JME-16-0080subject
Has Abstractpub_date
2016-08-01 00:00:00pages
F23-7issue
2eissn
0952-5041issn
1479-6813pii
JME-16-0080journal_volume
57pub_type
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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journal_title:Journal of molecular endocrinology
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