Progesterone and Estrogen Signaling in the Endometrium: What Goes Wrong in Endometriosis?

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AI-generated summary by claude@2026-06, 2026-06-07

This review examines molecular mechanisms of progesterone and estrogen signaling in the endometrium and how their dysregulation, particularly progesterone resistance and estrogen dominance, contributes to endometriosis pathology.

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Abstract

In the healthy endometrium, progesterone and estrogen signaling coordinate in a tightly regulated, dynamic interplay to drive a normal menstrual cycle and promote an embryo-receptive state to allow implantation during the window of receptivity. It is well-established that progesterone and estrogen act primarily through their cognate receptors to set off cascades of signaling pathways and enact large-scale gene expression programs. In endometriosis, when endometrial tissue grows outside the uterine cavity, progesterone and estrogen signaling are disrupted, commonly resulting in progesterone resistance and estrogen dominance. This hormone imbalance leads to heightened inflammation and may also increase the pelvic pain of the disease and decrease endometrial receptivity to embryo implantation. This review focuses on the molecular mechanisms governing progesterone and estrogen signaling supporting endometrial function and how they become dysregulated in endometriosis. Understanding how these mechanisms contribute to the pelvic pain and infertility associated with endometriosis will open new avenues of targeted medical therapies to give relief to the millions of women suffering its effects.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometrium Estrogens Progesterone Signal Transduction Animals Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Estrogens Female Hormones Hormones Hormones Humans Infertility, Female Infertility, Female Infertility, Female Progesterone

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References (100)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-12T06:13:51.797165+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:22:35.348889+00:00
License: CC0 · commercial use OK