Epigenetic regulation of the pathological process in endometriosis

Kuei‐Yang Hsiao, Meng-Hsing Wu, Meng‐Hsing Wu, Shaw‐Jenq Tsai
Reproductive medicine and biology · 2017 · vol. 16(4) , pp. 314–319 · doi:10.1002/rmb2.12047 · PMID:29259483 · W2736581470
review OA: gold CC0 ⤵ 53 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores how epigenetic modifications like DNA methylation, histone modification, and microRNA expression contribute to the development and maintenance of endometriosis.

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Abstract

Background: Endometriosis is one of the most common gynecological diseases that greatly compromises the quality of life in affected individuals. A growing body of evidence shows that the remodeling of retrograde endometrial tissues to the ectopic endometriotic lesions involves multiple epigenetic alterations, such as DNA methylation, histone modification, and microRNA expression. Methods: This article retrospectively reviewed the studies that were related to the epigenetic regulatory factors that contribute to the development and maintenance of endometriosis. A literature search was performed in order to collect scientific articles that were written in English by using the key words of "endometriosis," "epigenetics," "DNA methylation," "histone modification," and "microRNA." Results: Epigenetic modifications, including DNA methylation, histone modification, and microRNA expression, are involved in the pathogenesis of endometriosis. These epigenetic players are regulated or tuned by microenvironmental cues, such as locally produced estradiol, proinflammatory cytokines, and hypoxic stress, and reciprocally regulate the process or response to those stimuli. Conclusion: Understanding the molecular mechanisms that underlie these epigenetic regulatory processes would shed light on the etiology and/or progression of endometriosis and facilitate the development of novel therapeutic strategies.

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Condition tags

endometriosis

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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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