The elusive and controversial roles of estrogen and progesterone receptors in human endometriosis.

Ruijin Shao, Shujun Cao, Xiaoqin Wang, Yi Feng, Håkan Billig
American journal of translational research · 2014 · vol. 6(2) , pp. 104–13 · PMID:24489989 · PMC3902220 · W1560110733
article OA: green CC0 ⤵ 37 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review outlines studies examining the complex and often contradictory roles of estrogen and progesterone receptor subtypes and isoforms in the development and progression of endometriosis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This paper reviews evidence on how estrogen receptor (ERα/ERβ) and progesterone receptor (PRA/PRB) expression and regulation in human endometriosis lesions compare with normal eutopic endometrium, drawing on clinical in vivo studies and mechanistic data on hormone receptor subtype functions. Across studies, the authors highlight that results for ER subtype and PR isoform expression are conflicting, including reports of both decreased and unchanged or increased ERα/ERβ and PR variants across ovarian, peritoneal, and deep infiltrating endometriosis, and they note that relative ERβ:ERα ratios may shift even when absolute levels differ. A major caveat they emphasize is the inconsistency in human findings and the limited ability to define receptor roles in endometriosis given that animal models lack spontaneous endometriosis. This paper is centrally about endometriosis — specifically, it synthesizes controversial and heterogeneous roles of ER and PR subtypes/isoforms in endometriosis development and progression.

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Abstract

Endometriosis is a complex and challenging disease that involves aberrant adhesion, growth, and progression of endometrial tissues outside of the uterine cavity, and there is evidence to suggest that estrogen plays a key role in its development and progression. Numerous in vivo clinical studies have described the ectopic expression and regulation of estrogen receptor (ER) and progesterone receptor (PR) in the different types of endometriosis compared to normal or eutopic endometrium. However, we have noticed that conflicting and contradictory results have been presented in terms of ER subtype (ERα and ERβ) and PR isoform (PRA and PRB) expression. Both ER and PR are transcription factors and ER/PR-mediated responses depend on the coordinated, opposing, and compensatory functions of ER subtypes and PR isoforms. Moreover, analysis of the uterine phenotypes of ERα/ERβ and PRA/PRB knockout mice indicates that different ER subtypes and PR isoforms mediate distinct responses to steroid hormones and play different roles in uterine function. In this review, we outline studies that have elucidated the molecules and signaling pathways that are linked to ER and/or PR signaling pathways in the development and progression of endometriosis.

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endometriosis

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