Endometrial receptivity: lessons from systems biology and candidate gene studies of endometriosis

Begüm Aydoğan Mathyk, Begum Mathyk, Nyssa Adams, Steven L Young
Minerva ginecologica · 2017 · vol. 69(1) , pp. 41–56 · doi:10.23736/s0026-4784.16.03975-7 · PMID:27576850 · W2516080930
review OA: closed CC0 ⤵ 5 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

This review summarizes how progesterone resistance in endometriosis alters gene expression, transcription factors, proteins, and inflammatory mediators, impacting endometrial receptivity and embryo implantation.

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Abstract

Endometrial receptivity is essential for embryo implantation and ongoing successful pregnancy. The temporal "window" during which the endometrium allows implantation, known as window of implantation (WOI), which is, characterized alteration of many genes. Transcriptomic changes at the time of implantation let us discover many genes and their protein products whose altered expression effects endometrial receptivity. New omics technologies helped us to understand the complex dynamics of endometrium. Progesterone is responsible for decidualization and establishment of implantation. In women with endometriosis progesterone resistance might impair decidualization and subsequent implantation in different ways. We summarized the effects of progesterone resistance on genes, transcription factors, proteins and inflammatory mediators. Understanding the effects of progesterone resistance on genes and downstream targets will highlight future treatments in patients with endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Embryo Implantation Endometriosis Systems Biology Animals Embryo Implantation Endometriosis Endometrium Endometrium Female Humans Inflammation Mediators Inflammation Mediators Pregnancy Progesterone Progesterone Transcription Factors Transcription Factors Transcriptome Uterine Diseases

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.

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License: CC0 · commercial use OK