Reversal of fortune: estrogen receptor-β in endometriosis.
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.
Department of Physiology and BiophysicsUniversity of Arkansas for Medical Sciences, Little Rock, Arkansas, USA simmenrosalia@uams.edu.
Rosalia C M
RC
Simmen
Department of Obstetrics and GynecologyUniversity of Michigan Health System, Ann Arbor, Michigan, USA.
Angela S
AS
Kelley
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D004715:Endometriosis / Q000235:genetics / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism / Q000473:pathology; D047628:Estrogen Receptor alpha / Q000235:genetics / Q000378:metabolism; D047629:Estrogen Receptor beta / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D008954:Models, Biological; D011485:Protein Binding; D015398:Signal Transduction
D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D058847:Inflammasomes
apoptosome; endometriosis; estrogen receptor-beta; inflammation; non-genomic