Aberrant histone modification in endometriosis

Kaei Nasu, Yukie Kawano, Kentaro Kai, Yoko Aoyagi, Wakana Abe, Mamiko Okamoto, Hisashi Narahara
Frontiers in bioscience (Landmark edition) · 2014 · vol. 19(8) , pp. 1202 · doi:10.2741/4276 · W2014144126
review OA: bronze CC0 ⤵ 27 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review summarizes recent studies on aberrant histone acetylation patterns in endometriosis, including specific gene promoter hyper- and hypoacetylation, and discusses the potential therapeutic implications of epigenetic drugs.

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Abstract

Accumulating evidence suggests that epigenetic aberrations play definite roles in the pathogenesis of endometriosis. These include aberrations in genomic DNA methylation, microRNA expression, and histone modification. The aberrant histone modification status and the aberrant expression of histone deacetylases, which regulate histone acetylation, in endometriosis are the focus of this review. Herein, we summarize the recent studies in the following areas: (i) hyperacetylation of histones located in the promoter lesions of G-protein-coupled estrogen receptor 1, steroidogenic factor-1, and hypoxia-inducible factor-1 alpha genes and (ii) hypoacetylation of histones located in the promoter lesions of estrogen receptor alpha, homeobox A10, CCAAT/enhancer-binding protein alpha, p16INK4a, p21Waf1/Cip1, p27Kip1, checkpoint kinase 2, death receptor 6, and E-cadherin genes. Further research from the viewpoint of epigenetics may lead to the identification of the candidate molecules that are aberrantly expressed in endometriosis and may help elucidate the pathogenesis of this disease. In addition, epigenetic drugs (including histone deacetylase inhibitors) show promise for the treatment of endometriosis by amending the expression of these epigenetically dysregulated genes.
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Abstract

Accumulating evidence suggests that epigenetic aberrations play definite roles in the pathogenesis of endometriosis. These include aberrations in genomic DNA methylation, microRNA expression, and histone modification. The aberrant histone modification status and the aberrant expression of histone deacetylases, which regulate histone acetylation, in endometriosis are the focus of this review. Herein, we summarize the recent studies in the following areas: (i) hyperacetylation of histones located in the promoter lesions of G-protein-coupled estrogen receptor 1, steroidogenic factor-1, and hypoxia-inducible factor-1 alpha genes and (ii) hypoacetylation of histones located in the promoter lesions of estrogen receptor alpha, homeobox A10, CCAAT/enhancer-binding protein alpha, p16INK4a, p21Waf1/Cip1, p27Kip1, checkpoint kinase 2, death receptor 6, and E-cadherin genes. Further research from the viewpoint of epigenetics may lead to the identification of the candidate molecules that are aberrantly expressed in endometriosis and may help elucidate the pathogenesis of this disease. In addition, epigenetic drugs (including histone deacetylase inhibitors) show promise for the treatment of endometriosis by amending the expression of these epigenetically dysregulated genes.

Keywords

- Endometriosis - Histone Modification - Histone Deacetylase - Histone Deacetylase Inhibitor - Epigenetics - Review

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Epigenesis, Genetic Genetic Predisposition to Disease Histones Acetylation Endometriosis Female Gene Expression Regulation Genetic Predisposition to Disease Histones Humans Models, Genetic

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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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Cited by (27)

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