Dioxin and endometriosis: a new possible relation based on epigenetic theory

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This review explores the potential role of dioxin-induced epigenetic modifications in the development of endometriosis, a chronic gynecological condition.

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Abstract

Endometriosis is a chronic disease characterized by the growth of endometrial-like glands and stroma outside the uterine cavity. Nowadays, the exact etiology of endometriosis is unclear and the interaction between a variety of environmental physical and chemical compounds may potentially promote the disease in women with an individual susceptibility. The first demonstration of a relation between an environmental factor and endometriosis was obtained with the chronic dietary exposure of a primate colony to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Besides the well-known dioxin's pathway of action, several papers are focusing on the role of epigenetic mechanisms, a way through which the genome responds to the environment and can lead to permanent changes in gene expression until affecting the phenotypes or cause disease. In this review, we focus on the possible role of dioxin epigenetics modification in endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Dioxins Endometriosis Endometriosis Epigenesis, Genetic Animals Animals Dioxins Dioxins Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Epigenesis, Genetic Epigenesis, Genetic Epigenesis, Genetic Female Female

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 (68)

Cited by (22)

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