Endometriosis: harmful survival of an ectopic tissue

Janos Garai, János Garai, Valeria Molnar, Tamas Varga, Miklos Koppan, Attila Torok, Jozsef Bodis
Frontiers in bioscience : a journal and virtual library · 2006 · vol. 11(1) , pp. 595 · doi:10.2741/1821 · PMID:16146755 · W2031349419
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review details the pathogenesis of endometriosis, focusing on the implantation and survival of ectopic endometrial tissue, its contributing factors, and clinical aspects of diagnosis and management.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-10 ⓘ

This paper is a review describing how endometriosis arises from implantation of endometrial tissue outside the uterine cavity, often via retrograde menstruation, and how multiple interacting contributors—including genital tract abnormalities, genetic predisposition, hormonal imbalance, immune surveillance changes, inflammatory responses, and dysregulated endometrial cell behavior—may allow ectopic lesions to establish and persist. It summarizes proposed mediators that support survival and progression of endometriosis and links these processes to symptoms such as chronic pelvic pain and bleeding, as well as infertility risk and susceptibility to adenocarcinoma development. The authors note that genomic studies are beginning to delineate the diverse mediators and genetic background involved, and they discuss progress using transgenic animal models. This paper is centrally about endometriosis — it reviews the mechanisms underlying endometriotic lesion survival and progression.

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Abstract

Endometriosis results from implantation of endometrial tissue outside the uterine cavity. Endometriosis might remain asymptomatic and discovered accidentally. However, it may cause symptoms, which include chronic pelvic pain, bleeding, infertility, and increases susceptibility to development of adenocarcinoma. The most prevailing hypothesis is that endometriosis results from implantation of endometrial tissue that gains access to peritoneal cavity by retrograde flow during menstruation. The factors contributing to the establishment and persistence of the endometriotic lesions (plaques) most probably include abnormalities of the genital tract, genetic predisposition, hormonal imbalance, altered immune surveillance, inflammatory response and abnormal regulation of the endometrial cells. The mediators that contribute to survival and progression of endometriosis are likely involved in the development of the symptoms of this process. Genomic studies have started to delineate the wide array of mediators involved and the complex genetic background required in the development of endometriosis. This review summarizes our current knowledge regarding the pathogenesis of endometriosis, including progress made with transgenic animals, and a clinical perspective on the diagnosis and management of this common process.

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Condition tags

mesh:D004715mesh:D017699endometriosischronic_pelvic_paininfertility

MeSH descriptors

Endometriosis Endometriosis Animals Animals, Genetically Modified Choristoma Choristoma Endometrial Neoplasms Endometrial Neoplasms Endometrial Neoplasms Endometriosis Endometriosis Endometrium Endometrium Estrogens Estrogens Female Humans Immune System Infertility, Female Infertility, Female

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 (40)

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