Epigenetic modifications working in the decidualization and endometrial receptivity.

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This review examines how epigenetic modifications, including DNA methylation and non-coding RNAs, regulate decidualization and endometrial receptivity to address reproductive disorders.

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This review examines the role of epigenetic modifications, including DNA methylation, histone modification, and non-coding RNAs, in regulating gene expression during human endometrial decidualization. The authors highlight how these molecular mechanisms coordinate with steroid hormones and growth factors to ensure proper blastocyst implantation and placental development, noting that deficient decidualization is linked to reproductive disorders. A key limitation noted is the reliance on emerging evidence, which suggests a need for further research to translate these findings into clinical predictions and treatments for pregnancy complications. Relevance to endometriosis: listed as one indication for GnRH antagonists, though the paper's main focus is uterine fibroids.

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Abstract

Decidualization is a critical event for the blastocyst implantation, placental development and fetal growth and the normal term. In mice, the embryo implantation to the uterine epithelial would trigger the endometrial stromal cells to differentiate into decidual stromal cells. However, decidualization in women takes place from the secretory phase of each menstrual cycle and continues to early pregnancy if there is conceptus. Deficient decidualization is often associated with pregnancy specific complications and reproductive disorders. Dramatic changes occur in the gene expression profiles during decidualization, which is coordinately regulated by steroid hormones, growth factors, and molecular and epigenetic mechanisms. Recently, emerging evidences showed that epigenetic modifications, mainly including DNA methylation, histone modification, and non-coding RNAs, play an important role in the decidualization process via affecting the target genes' expression. In this review, we will focus on the epigenetic modifications in decidualization and open novel avenues to predict and treat the pregnancy complications caused by abnormal decidualization.
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Abstract

Decidualization is a critical event for the blastocyst implantation, placental development and fetal growth and the normal term. In mice, the embryo implantation to the uterine epithelial would trigger the endometrial stromal cells to differentiate into decidual stromal cells. However, decidualization in women takes place from the secretory phase of each menstrual cycle and continues to early pregnancy if there is conceptus. Deficient decidualization is often associated with pregnancy specific complications and reproductive disorders. Dramatic changes occur in the gene expression profiles during decidualization, which is coordinately regulated by steroid hormones, growth factors, and molecular and epigenetic mechanisms. Recently, emerging evidences showed that epigenetic modifications, mainly including DNA methylation, histone modification, and non-coding RNAs, play an important role in the decidualization process via affecting the target genes’ expression. In this review, we will focus on the epigenetic modifications in decidualization and open novel avenues to predict and treat the pregnancy complications caused by abnormal decidualization. Similar content being viewed by others

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Life Sci. 77, 2091–2101 (2020). https://doi.org/10.1007/s00018-019-03395-9 Received: Revised: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s00018-019-03395-9

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