Homeostasis Imbalance in the Endometrium of Women with Implantation Defects: The Role of Estrogen and Progesterone

Bruce A Lessey, Steven L Young
Seminars in reproductive medicine · 2014 · vol. 32(05) , pp. 365–375 · doi:10.1055/s-0034-1376355 · PMID:24959818 · W1994082744
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review examines how estrogen and progesterone imbalance and defective inflammation resolution in endometriosis lead to implantation defects and suggests estrogen action as a therapeutic target.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This review examines how embryo implantation depends on a regulated inflammatory process that is sequentially activated and then resolved by estrogen and progesterone, mediated through steroid receptors, cofactors, chaperones, and downstream signaling pathways. It highlights that endometriosis is associated with prematurely activated, menstruation-like inflammatory cascades in eutopic endometrium and with defective mechanisms for inflammation resolution, alongside a shift from normal luteal-phase progesterone dominance toward progesterone resistance and estrogen dominance. A major caveat is that, as a narrative review, it synthesizes evidence and mechanisms rather than presenting original experimental or clinical data with study-level inclusion criteria. Relevance to endometriosis: it explicitly frames endometriosis as a condition where inflammatory cascades are prematurely activated and where estrogen/progesterone imbalance and resolution failure are linked to implantation failure, though the paper is primarily a mechanistic review of estrogen and progesterone’s roles in implantation and chronic inflammation.

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Abstract

Embryo implantation is regulated by an inflammatory process in response to sequential exposure to estrogen and progesterone, followed by resolution and repair. The actions of estrogen and progesterone on these inflammatory processes are tightly and reciprocally controlled through regulated expression of steroid receptors, cofactors, chaperone proteins, and downstream signaling components. In endometriosis, the inflammatory cascades, normally seen at menstruation, are prematurely activated and endogenous endometrial mechanisms of inflammation resolution appear defective. The temporally abnormally inflammation is also associated with an imbalance between estrogen and progesterone actions; the normal luteal-phase dominance of progesterone action appears to be lost and is replaced by progesterone resistance and estrogen dominance. In this review, we examine these relationships in greater detail and argue that estrogen action is a prime target for future therapeutic solutions to endometriosis and implantation failure that result from this chronic, inflammatory disease.

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Condition tags

endometriosis

MeSH descriptors

Embryo Implantation Endometrium Estrogens Homeostasis Infertility, Female Progesterone Embryo Implantation Endometriosis Endometriosis Endometriosis Endometrium Endometrium Estrogens Female Homeostasis Humans Infertility, Female Infertility, Female Progesterone

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

Cited by (33)

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License: CC0 · commercial use OK