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Full list of author information is available at the end of the articleBackground Endometriosis is a steroid-dependent condition defined by the presence of endometrial tissue outside of the uterine cavity resulting in diverse clinical manifesta-tions, such as infertility, pelvic pain, and dysmenorrhea [1]. Endometriosis affects 3%–10 % of reproductive-aged women and 20%–50 % of women with infertility [2]. Sus-ceptibility to endometriosis is dependent on a complex interaction of genetic, immunological, and hormonal fac-tors [3-5]; however, the exact etiology and pathogenesis of the disease remain unclear. Estrogen has been shown to play a critical role in the growth of endometriotic tissues [6]. By binding to the estrogen receptor (ER), estrogen triggers a broad array of tissue and organ-specific physiological responses. There are two isoforms of ERs, ER-α and ER-β, which exhibi