Molecular dysregulations underlying the pathogenesis of endometriosis

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This paper investigates the molecular abnormalities contributing to the development of endometriosis, aiming to identify key pathways and cellular processes involved.

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Abstract

Endometriosis is a crippling disease characterized by the presence of endometrium-like tissue or scar outside the uterine cavity, commonly confined to the peritoneal and serosal surfaces of the pelvic organs. 10-15% of women in reproductive age are estimated to be affected by endometriosis. Most of these patients present with infertility and suffer from pelvic pain. The benign disease rarely progresses to malignancy. Regardless of its high prevalence, the pathogenesis of the disease is not fully understood. Treatment options for endometriosis are limited and are often based on a symptomatic approach. The unavailability of proper diagnostic approaches, fewer therapeutic options, and sparse understanding of molecular alterations are responsible for the continued disease burden. Exploring the molecular elements causing the pathogenesis of endometriosis may lead to a number of breakthroughs in the treatment of the illness, such as the discovery of new biomarkers for diagnosis and therapeutic targets that can be a guide to better prognosis and reduced recurrence. The goal of this review is to provide the reader a critical understanding of the disease by summarizing the genetic, immunological, hormonal, and epigenetic deregulations that support the molecular basis for development of endometriotic cyst, with a special focus on the study models needed to analyze these changes in the endometriotic microenvironment.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Neoplasms Neoplasms Biomarkers Endometrium Endometrium Female Humans Tumor Microenvironment

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.

References (100)

Cited by (12)

Source provenance

europepmc
last seen: 2026-09-27T09:11:36.575535+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:24:20.309598+00:00
unpaywall
last seen: 2026-09-29T06:34:56.587159+00:00
License: CC0 · commercial use OK