Reversal of fortune: estrogen receptor-β in endometriosis

    1. Angela S Kelley2
    1. 1Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    2. 2Department of Obstetrics and Gynecology, University of Michigan Health System, Ann Arbor, Michigan, USA
    1. Correspondence should be addressed to R C M Simmen; Email: simmenrosalia{at}


    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.

    • Received 27 May 2016
    • Accepted 7 June 2016
    • Made available online as an Accepted Preprint 1 August 2016
    | Table of Contents