A current view of the role of epigenetic changes in the aetiopathogenesis of endometriosis

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Epigenetic changes are central to the hormonal, immunological, and inflammatory aberrations driving endometriosis aetiopathogenesis, with their breakdown initiating the disease's formation.

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Abstract

The purpose of the study was to examine the role of epigenetic changes in the aetiopathogenesis of endometriosis. The analysis and review of the relevant current literature in English language related to the role of epigenetic changes in the aetiopathogenesis of endometriosis. Epigenetic changes are common denominators for hormonal, immunological and inflammatory aberrations which play a key role in the aetiopathogenesis of endometriosis. Many internal and external factors may cause the different running of the epigenetic mechanism. As yet fully unknown genetic factors may increase the sensitivity of the epigenetic mechanism to various internal and external factors. The breakdown of epigenetic regulation is the main factor initiating the pathogenetic mechanisms for endometriosis formation.

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Condition tags

endometriosis

MeSH descriptors

Autoimmunity Endometriosis Epigenesis, Genetic Epigenesis, Genetic Gonadal Steroid Hormones Inflammation Autoimmunity Autoimmunity CpG Islands CpG Islands DNA Methylation DNA Methylation Endometriosis Endometriosis Endometriosis Female Female Gonadal Steroid Hormones Gonadal Steroid Hormones Humans

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (89)

Cited by (10)

Source provenance

europepmc
last seen: 2026-10-16T06:09:50.462052+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:16:31.290043+00:00
License: CC0 · commercial use OK