子宫内膜异位症发病机制中的染色质修饰因子

Q3 Medicine
K. A. Abaeva, R. T. Murtazova, I. A. Vaniev, A. V. Lazarova, A. A. Sozaeva, M. A. Gogichaeva, A. A. Pirozhnikova, K. V. Ignashev, M. S. Dadashov, D. V. Kolesnikova, A. A. Bayramova, V. E. Kucherskaya, L. D. Zulfalieva, A. M. Zaitseva
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The search was conducted in the databases PubMed, Scopus, Web of Science, Google Scholar and eLibrary. Keywords and phrases in Russian and English related to the research topic were used as follows: \"endometriosis\", \"chromatin modifiers\", \"histone acetylation\", \"DNA methylation\", \"microRNA\", \"endometriosis\", \"chromatin modifiers\", \"histone acetylation\", \"DNA methylation\", \"microRNA\". The evaluation of articles was carried out in accordance with PRISMA recommendations.Results. Chromatin modifiers control differentiation, growth and development, aging and cell death by interacting with various functional chromatin elements. They can cause abnormal gene expression by regulating chromatin structure affecting emergence and development of endometriosis. DNA methylation determines cell types, controls gene expression and genome stability. Abnormal DNA methylation in gene promoter regions necessary for normal endometrial response affects endometriosis development. DNA methyltransferase (DNMT) inhibitors reduce the methylation of human homeobox A10 (HOXA10) and progesterone receptor (PR) genes and potentiate their expression in endometrial cells, improving endometrial susceptibility and inhibiting cell cycle progression. Abnormal histone modifications in endometrial cells may facilitate or hinder the access of transcription mechanisms to chromatin DNA. Histone deacetylase inhibitors effectively eliminate the effects of abnormal histone modifications in endometriosis cells and prevent endometriosis progression. The expression of non-coding RNAs and chromatin remodeling complexes also alters chromatin structure being involved in arising endometriosis and is associated with infertility by promoting proliferation, invasion and migration of endometriod cells.Conclusion. Chromatin modifiers play a key role in developing endometriosis by controlling gene expression and chromatin structure. 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引用次数: 0

摘要

导言。研究发现,各种表观遗传学异常可能在子宫内膜异位症的发病机制中扮演重要角色。染色质结构的调控主要由染色质修饰剂(CMs)进行,它们通过发挥预期的生物学功能和引起表观遗传学变化,刺激具有不同功能结构的基因组区域的生成,从而改变基因表达的模式或水平。目的:通过评估目前的出版物,探讨СМs在子宫内膜异位症发病机制中的作用及其调控机制。在 PubMed、Scopus、Web of Science、Google Scholar 和 eLibrary 等数据库中进行了搜索。与研究主题相关的俄语和英语关键词和短语如下:"子宫内膜异位症"、"染色质修饰剂"、"组蛋白乙酰化"、"DNA 甲基化"、"microRNA"、"子宫内膜异位症"、"染色质修饰剂"、"组蛋白乙酰化"、"DNA 甲基化"、"microRNA"。根据 PRISMA 建议对文章进行了评估。染色质修饰因子通过与各种功能性染色质元素相互作用来控制分化、生长发育、衰老和细胞死亡。它们可通过调节染色质结构导致基因表达异常,从而影响子宫内膜异位症的出现和发展。DNA 甲基化决定细胞类型,控制基因表达和基因组稳定性。正常子宫内膜反应所需的基因启动子区域的 DNA 甲基化异常会影响子宫内膜异位症的发生。DNA 甲基转移酶(DNMT)抑制剂可减少人类同源染色体 A10(HOXA10)和孕酮受体(PR)基因的甲基化,并增强其在子宫内膜细胞中的表达,从而改善子宫内膜的易感性并抑制细胞周期的进展。子宫内膜细胞中异常的组蛋白修饰可能会促进或阻碍转录机制进入染色质 DNA。组蛋白去乙酰化酶抑制剂能有效消除子宫内膜异位症细胞中异常组蛋白修饰的影响,防止子宫内膜异位症的进展。非编码 RNA 和染色质重塑复合物的表达也会改变染色质结构,参与子宫内膜异位症的发生,并通过促进子宫内膜异位细胞的增殖、侵袭和迁移与不孕症有关。染色质修饰因子通过控制基因表达和染色质结构,在子宫内膜异位症的发病过程中发挥着关键作用。了解其潜在机制可为诊断和开发治疗子宫内膜异位症的新方法提供有价值的信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chromatin modifiers in endometriosis pathogenesis
Introduction. It was revealed that various epigenetic abnormalities may play an important role in the endometriosis pathogenesis. The regulation of chromatin structure is carried out mainly by chromatin modifiers (CMs), which stimulate generation of genomic regions with different functional structures and thus change the patterns or levels of gene expression by exerting expected biological functions and causing epigenetic changes.Aim: to consider СМs role in endometriosis pathogenesis and their regulation mechanism assessing current publications.Materials and Methods. The search was conducted in the databases PubMed, Scopus, Web of Science, Google Scholar and eLibrary. Keywords and phrases in Russian and English related to the research topic were used as follows: "endometriosis", "chromatin modifiers", "histone acetylation", "DNA methylation", "microRNA", "endometriosis", "chromatin modifiers", "histone acetylation", "DNA methylation", "microRNA". The evaluation of articles was carried out in accordance with PRISMA recommendations.Results. Chromatin modifiers control differentiation, growth and development, aging and cell death by interacting with various functional chromatin elements. They can cause abnormal gene expression by regulating chromatin structure affecting emergence and development of endometriosis. DNA methylation determines cell types, controls gene expression and genome stability. Abnormal DNA methylation in gene promoter regions necessary for normal endometrial response affects endometriosis development. DNA methyltransferase (DNMT) inhibitors reduce the methylation of human homeobox A10 (HOXA10) and progesterone receptor (PR) genes and potentiate their expression in endometrial cells, improving endometrial susceptibility and inhibiting cell cycle progression. Abnormal histone modifications in endometrial cells may facilitate or hinder the access of transcription mechanisms to chromatin DNA. Histone deacetylase inhibitors effectively eliminate the effects of abnormal histone modifications in endometriosis cells and prevent endometriosis progression. The expression of non-coding RNAs and chromatin remodeling complexes also alters chromatin structure being involved in arising endometriosis and is associated with infertility by promoting proliferation, invasion and migration of endometriod cells.Conclusion. Chromatin modifiers play a key role in developing endometriosis by controlling gene expression and chromatin structure. Understanding underlying mechanisms provides valuable information for diagnostics and development of new approaches to treat endometriosis.
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