Estrogen Receptor-β Signaling in Endometriosis

Endometriosis is responsible for dysmenorrhea, chronic pelvic pain, infertility and obstetric complications, and it affects approximately 10-20% of women of reproductive age. Endometriosis is known as estrogen-dependent inflammatory disorder while the pathogenesis remains unclear. Pathological theories of retrograde menstruation, Müllerian remnants, stem cell and coelomic metaplasia have been postulated. The most effective medical treatment in managing symptomatic endometriosis is to induce a hypo-estrogenic status but patients might present with severe menopausal-like side effects, such as hot flush, insomnia or osteoporosis. Because of high recurrence rate of endometriosis, patients with severe endometriosis might receive repeat operations even after successive medical or surgical treatments. Recent studies have revealed the role of estrogen receptor-β (ER-β) in the pathogenesis of endometriosis which involved inflammation, adhesion, anti-apoptosis and cell proliferation. In this review, we aim to condense the role of ER-β in the pathogenesis of endometriosis.