| Literature DB >> 27272520 |
Rosalia C M Simmen1, Angela S Kelley2.
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.Entities:
Keywords: apoptosome; endometriosis; estrogen receptor-beta; inflammation; non-genomic
Mesh:
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Year: 2016 PMID: 27272520 PMCID: PMC4973618 DOI: 10.1530/JME-16-0080
Source DB: PubMed Journal: J Mol Endocrinol ISSN: 0952-5041 Impact factor: 5.098