Estrogen Receptor-β Signaling in Endometriosis

Ben‐Shian Huang
In: Adaptive Medicine · 2018 · vol. 10(1) , pp. 10–15 · doi:10.4247/am.2018.abh192 · W2802516764
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-07-09 ⓘ

This review condenses current research on the role of estrogen receptor-β in the pathogenesis of endometriosis, including its involvement in inflammation, adhesion, anti-apoptosis, and cell proliferation.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-09 · read from full text ⓘ

This open-access review examines endometriosis as an estrogen-dependent inflammatory disorder and synthesizes evidence on how estrogen receptor-β (ER-β) contributes to endometriosis pathogenesis. It describes proposed upstream theories for endometriosis development and discusses current medical approaches that induce a hypo-estrogenic state while noting the potential for menopausal-like side effects and high recurrence leading to repeat surgeries. The review reports that ER-β has been implicated in processes including inflammation, adhesion, anti-apoptosis, and cell proliferation. This paper is centrally about endometriosis — it specifically condenses the role of ER-β signaling in endometriosis pathogenesis.

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Abstract

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.
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- 期刊 - OpenAccess 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.

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endometriosischronic_pelvic_paindysmenorrheainfertility

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