Endometriosis and Epigenetics: What do we Know?

Joseph Nassif, Ali Khalil, Naji Aswad, Antoine Abu Musa, Georges Rameh
In: Women's Health - Open Journal · 2018 · vol. 4(1) , pp. 1–7 · doi:10.17140/whoj-4-125 · W2914371440
article OA: diamond CC0
🔓 Open OA copy Full text JSON View on OpenAlex View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This review explores the multiplicity of epigenetic changes associated with the complex and not fully understood pathogenesis of endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by qwen3.7-flash, 2026-09-27 · read from full text ⓘ

This review examines the multifactorial pathogenesis of endometriosis by exploring various epigenetic alterations that contribute to disease progression. The authors categorize these changes into DNA methylation, microRNA dysregulation, immunologic modifications, and histone acetylation, noting their cross-reactions with genetic and environmental factors. Key findings indicate that DNA hypomethylation and hypermethylation influence gene transcription, while miRNAs regulate RNA processes and immune cell function is impaired through downregulation. The paper concludes that understanding these complex epigenetic pathways may lead to the development of more effective treatments for the condition. This paper is centrally about endometriosis — specifically focusing on the role of epigenetic mechanisms in its pathogenesis and potential therapeutic targeting.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is a common gynecological condition with a pathogenesis that is multifactorial and not well understood. The aim of this review was to explore the multiplicity of epigenetic changes in the field of this disease.
Full text 1,279 characters · extracted from oa-html · 3 sections · click to expand

Keywords

Endometriosis; Epigenetics; DNA methylation; Histone acetylation; Immunologic dysregulation; micro RNA expressionAbstract

Objective

Endometriosis is a common gynecological condition with a pathogenesis that is multifactorial and not well understood. The aim of this review was to explore the multiplicity of epigenetic changes in the field of this disease. Main Findings Epigenetic alterations in endometriosis may be classified into four main categories, with cross-reactions between these changes as well as genetic, environmental, hormonal factors, etc. Deoxyribonucleic acid (DNA) hypomethylation and hypermethylation control the transcription of several genes leading to the progression of this condition. Micro RNAs (miRNA) dysregulation controls ribonucleic acid (RNA) translation, degradation, and splicing. Immunologic changes involved downregulate the ability of immune cells to target shed cells. Furthermore, histone hypoacetylation and hyperacetylation affect the metabolism of steroids.

Conclusion

Endometriosis pathogenesis is a very wide and complex subject, associating several hypotheses. The epigenetic pathways discussed in this review may be the target of new more effective treatments in this field.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-html ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

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 (32)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK