■评估当前文献评估人类子宫内膜异位症的表观遗传学。
■根据PubMed中的PRISMA指南进行了系统审查,EBSCOhost,科克伦图书馆,Embase,Scopus,和WebofScience核心合集。数据信息员制定了全面的搜索策略。截至1月15日,评估人类表观遗传学的观察和介入研究以英文发表,2023年,包括。两名评审员独立筛选评估表观遗传学在子宫内膜异位症中作用的研究。使用CochraneRoB2.0工具和纽卡斯尔-渥太华量表评估偏倚风险。提取的数据进行描述性分析。
■我们确定了18.639项研究,其中包括57个,包括1.623例子宫内膜异位症患者和1.243例对照。在包括的57项研究中,50项(88%)为病例对照研究,和7(12%)是横截面。59%的研究是亚洲人,25%来自美国14%是欧洲人,2%来自非洲。乙酰化和甲基化是本综述集中的两个主要的关键组蛋白修饰。因此,我们将这些研究分为关注全基因组甲基化和组蛋白乙酰化的研究.几项研究发现子宫内膜异位症与高甲基化基因之间存在关联,包括PGR-B,SF-1和RASSF1A。HOXA10,COX-2,IL-12B,一些研究发现子宫内膜异位组织中GATA6低甲基化。关于组蛋白修饰,多项研究报道,组蛋白H3和H4的乙酰化水平影响与子宫内膜异位症相关的多个基因.此外,在两项研究中发现子宫内膜异位症患者中HDAC2升高。
■一些研究报道了子宫内膜活检和正常组织中特定基因甲基化水平之间的显著差异,这表明DNA甲基化可能在子宫内膜异位组织基因型的调节中起重要作用。乙酰化和甲基化是导致子宫内膜异位组织中差异基因表达的两个关键组蛋白修饰。这57项研究报告的基因表达变化可能对细胞周期生长有直接影响。细胞周期停滞,和细胞凋亡,因此,可能在子宫内膜异位症的发病机制中起关键作用。这篇综述提供了以下见解:组蛋白修饰需要进一步研究,以评估其作为子宫内膜异位症潜在生物标志物和治疗靶标的作用。尽管报道了几个关键的相似之处,结果之间存在一些分歧,这可能归因于研究之间的异质性。需要更可靠的标准化的进一步研究来验证子宫内膜异位症的表观遗传变化。
UNASSIGNED: To assess the current literature evaluating the epigenetics of endometriosis in humans.
UNASSIGNED: A systematic
review was conducted in accordance with the PRISMA guidelines within PubMed, EBSCOhost, Cochrane Library, Embase, Scopus, and Web of Science Core Collection. A comprehensive search strategy was developed by a data informationist. Observational and interventional studies assessing epigenetics in humans published in English up to January 15th, 2023, were included. Two reviewers independently screened studies evaluating the role of epigenetics in endometriosis. The risk of bias was assessed using Cochrane RoB 2.0 tool and the Newcastle-Ottawa scale. Extracted data were analyzed descriptively.
UNASSIGNED: We identified 18.639 studies, of which 57 were included, comprising 1.623 patients with endometriosis and 1.243 controls. Among the 57 studies included, 50 (88%) were case-control studies, and 7 (12%) were cross-sectional. Fifty-nine percent of the studies were Asian, 25% were from America, 14% were European, and 2% were from Africa. Acetylation and methylation were the two main key histone modifications that were centered in this
review. Accordingly, we classified the studies as those focusing on genome-wide methylation and those on histone acetylation. Several studies identified an association between endometriosis and hypermethylated genes, including the PGR-B, SF-1, and RASSF1A. The genes HOXA10, COX-2, IL-12B, and GATA6 were found to be hypomethylated in endometriotic tissue by several studies. In regards to histone modification, multiple studies reported that the acetylation levels of histones H3 and H4 affect multiple genes associated with endometriosis. In addition, HDAC2 was found to be elevated in endometriosis patients in two studies.
UNASSIGNED: Several studies reported a significant difference between specific genes\' methylation levels in endometrial biopsies and normal tissue, which suggests that DNA methylation may play an important role in the modulation of the genotype in endometriotic tissue. Acetylation and methylation are the two key histone modifications leading to differential gene expression in endometriotic tissues. The alterations in gene expression reported by the 57 studies can have direct implications on cell cycle growth, cell cycle arrest, and apoptosis and, therefore, might play a key role in the pathogenesis of endometriosis. This
review offers insight that histone modifications need further research to evaluate their role as potential biomarkers and treatment targets for endometriosis. Although several key similarities were reported, there were some disagreements among the results, which might be attributable to the heterogeneity between studies. Further research with a more robust standardization is needed to validate the epigenetic changes in endometriosis.