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Epigenetic regulation of the pathological process in endometriosis.
Hsiao, Kuei-Yang; Wu, Meng-Hsing; Tsai, Shaw-Jenq.
Afiliação
  • Hsiao KY; Department of Physiology College of Medicine National Cheng Kung University Tainan Taiwan.
  • Wu MH; Department of Obstetrics and Gynecology College of Medicine National Cheng Kung University Tainan Taiwan.
  • Tsai SJ; Department of Physiology College of Medicine National Cheng Kung University Tainan Taiwan.
Reprod Med Biol ; 16(4): 314-319, 2017 10.
Article em En | MEDLINE | ID: mdl-29259483
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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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2017 Tipo de documento: Article