AI Article Synopsis
- * Changes in estrogen receptor-alpha (ERα) and estrogen receptor-beta (ERβ) are observed when normal endometrial cells transform into these ectopic lesions.
- * Recent research suggests that ERβ is linked to the disruption of apoptotic and inflammatory networks in endometriosis, indicating the importance of understanding these nongenomic actions in order to identify key regulatory pathways involved in the disease's development and advancement.
Article 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.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4973618 | PMC |
| http://dx.doi.org/10.1530/JME-16-0080 | DOI Listing |
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