Reversal of Fortune: Estrogen Receptor-Beta in Endometriosis

Abstract

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.