Estrogen receptor function: impact on the human endometrium
File(s)
Published version
Author(s)
Type
Journal Article
Abstract
The physiological role of estrogen in the female endometrium is well established. On the basis of responses to steroid hormones (progesterone, androgen, and estrogen), the endometrium is considered to have proliferative and secretory phases. Estrogen can act in the endometrium by interacting with estrogen receptors (ERs) to induce mucosal proliferation during the proliferative phase and progesterone receptor (PR) synthesis, which prepare the endometrium for the secretory phase. Mouse knockout studies have shown that ER expression, including ERα, ERβ, and G-protein-coupled estrogen receptor (GPER) in the endometrium is critical for normal menstrual cycles and subsequent pregnancy. Incorrect expression of ERs can produce many diseases that can cause endometriosis, endometrial hyperplasia (EH), and endometrial cancer (EC), which affect numerous women of reproductive age. ERα promotes uterine cell proliferation and is strongly associated with an increased risk of EC, while ERβ has the opposite effects on ERα function. GPER is highly expressed in abnormal EH, but its expression in EC patients is paradoxical. Effective treatments for endometrium-related diseases depend on understanding the physiological function of ERs; however, much less is known about the signaling pathways through which ERs functions in the normal endometrium or in endometrial diseases. Given the important roles of ERs in the endometrium, we reviewed the published literature to elaborate the regulatory role of estrogen and its nuclear and membrane-associated receptors in maintaining the function of endometrium and to provide references for protecting female reproduction. Additionally, the role of drugs such as tamoxifen, raloxifene, fulvestrant and G-15 in the endometrium are also described. Future studies should focus on evaluating new therapeutic strategies that precisely target specific ERs and their related growth factor signaling pathways.
Date Issued
2022-02-28
Date Acceptance
2022-02-01
Citation
Frontiers in Endocrinology, 2022, 13
ISSN
1664-2392
Publisher
Frontiers Media S.A.
Journal / Book Title
Frontiers in Endocrinology
Volume
13
Copyright Statement
© 2022 Yu, Huang, Xu, Li, Fu and Deng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
License URL
Identifier
https://www.ncbi.nlm.nih.gov/pubmed/35295981
Subjects
ACTIVATION FUNCTION
ALPHA ER-ALPHA
CELL-PROLIFERATION
Endocrinology & Metabolism
endometrium
estrogen receptor alpha
estrogen receptor beta
GPER EXPRESSION
G-protein-coupled estrogen receptor
GROWTH-FACTOR RECEPTOR
human
Life Sciences & Biomedicine
MESSENGER-RNA EXPRESSION
PROGESTERONE ACTION
PROTEIN-COUPLED RECEPTOR
RIBONUCLEIC-ACID
Science & Technology
STRUCTURAL BASIS
Publication Status
Published
Coverage Spatial
Switzerland
Article Number
827724
Date Publish Online
2022-02-28