{"title":"探索血清素转运子启动子区甲基化水平与抑郁症状之间的关系:一项系统综述和多层次荟萃分析","authors":"F Javelle, G Dao, M Ringleb, W Pulverer, W Bloch","doi":"10.1038/s41398-025-03356-w","DOIUrl":null,"url":null,"abstract":"<p><p>Depressive disorders result from complex interactions among genetic, epigenetic, and environmental factors. DNA methylation, a key epigenetic mechanism, is crucial in understanding depressive symptoms development. The serotonin transporter gene (5-HTT) and its polymorphisms, like 5-HTTLPR, have been extensively studied in relation to depression, yet conflicting findings regarding the association between 5-HTT promoter methylation and depressive symptoms persist, largely due to methodological differences. Thus, this systematic review and meta-analysis aims to assess (1) 5-HTT promoter methylation levels between depressed and non-depressed conditions and (2) the association between 5-HTT methylation and depressive symptoms severity. We searched PubMed, Google Scholar, and Web of Science from inception to January 15th, 2025 (PROSPERO: CRD42023355414) and performed two independent multi-level meta-analyses to answer our aims. Twenty-four trials were included in the systematic review. All reported effects carried potential for bias. The meta-analysis for depression occurrence (12 studies - 2028 subjects - 127 effects) indicated no significant effect (Hedges'g = 0.06) with moderate within- and low between-study heterogeneity. The depression severity analysis (14 studies - 2296 subjects - 116 effects) revealed a null effect size (Fisher's Z = 0.05), with no within- and moderate between-study heterogeneity. Asymmetry was detected for both meta-analyses. Moderator analyses demonstrated no significant effects of depression severity, methylation techniques, single-CpG sites, cell types assessed, age, and female percentage. This comprehensive review provides insights into the intricate interplay between 5-HTT promoter methylation and depressive symptoms. Furthermore, it offers well-considered recommendations for future research endeavors and delineates guidelines for reporting methylation research.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"161"},"PeriodicalIF":5.8000,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049537/pdf/","citationCount":"0","resultStr":"{\"title\":\"Exploring the association between serotonin transporter promoter region methylation levels and depressive symptoms: a systematic review and multi-level meta-analysis.\",\"authors\":\"F Javelle, G Dao, M Ringleb, W Pulverer, W Bloch\",\"doi\":\"10.1038/s41398-025-03356-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Depressive disorders result from complex interactions among genetic, epigenetic, and environmental factors. DNA methylation, a key epigenetic mechanism, is crucial in understanding depressive symptoms development. The serotonin transporter gene (5-HTT) and its polymorphisms, like 5-HTTLPR, have been extensively studied in relation to depression, yet conflicting findings regarding the association between 5-HTT promoter methylation and depressive symptoms persist, largely due to methodological differences. Thus, this systematic review and meta-analysis aims to assess (1) 5-HTT promoter methylation levels between depressed and non-depressed conditions and (2) the association between 5-HTT methylation and depressive symptoms severity. We searched PubMed, Google Scholar, and Web of Science from inception to January 15th, 2025 (PROSPERO: CRD42023355414) and performed two independent multi-level meta-analyses to answer our aims. Twenty-four trials were included in the systematic review. All reported effects carried potential for bias. The meta-analysis for depression occurrence (12 studies - 2028 subjects - 127 effects) indicated no significant effect (Hedges'g = 0.06) with moderate within- and low between-study heterogeneity. The depression severity analysis (14 studies - 2296 subjects - 116 effects) revealed a null effect size (Fisher's Z = 0.05), with no within- and moderate between-study heterogeneity. Asymmetry was detected for both meta-analyses. Moderator analyses demonstrated no significant effects of depression severity, methylation techniques, single-CpG sites, cell types assessed, age, and female percentage. This comprehensive review provides insights into the intricate interplay between 5-HTT promoter methylation and depressive symptoms. Furthermore, it offers well-considered recommendations for future research endeavors and delineates guidelines for reporting methylation research.</p>\",\"PeriodicalId\":23278,\"journal\":{\"name\":\"Translational Psychiatry\",\"volume\":\"15 1\",\"pages\":\"161\"},\"PeriodicalIF\":5.8000,\"publicationDate\":\"2025-05-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12049537/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Translational Psychiatry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41398-025-03356-w\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PSYCHIATRY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational Psychiatry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41398-025-03356-w","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PSYCHIATRY","Score":null,"Total":0}
引用次数: 0
摘要
抑郁症是遗传、表观遗传和环境因素复杂相互作用的结果。DNA甲基化是一种关键的表观遗传机制,对理解抑郁症状的发展至关重要。5-羟色胺转运体基因(5-HTT)及其多态性,如5-HTTLPR,已经被广泛地研究与抑郁症的关系,然而,关于5-HTT启动子甲基化与抑郁症状之间的关系的矛盾发现仍然存在,主要是由于方法上的差异。因此,本系统综述和荟萃分析旨在评估(1)抑郁和非抑郁状态下5-HTT启动子甲基化水平和(2)5-HTT甲基化与抑郁症状严重程度之间的关系。我们检索了PubMed, b谷歌Scholar和Web of Science从成立到2025年1月15日(PROSPERO: CRD42023355414),并进行了两个独立的多水平元分析来回答我们的目标。系统评价纳入了24项试验。所有报道的效应都可能存在偏倚。抑郁症发生的荟萃分析(12项研究- 2028名受试者- 127项影响)显示无显著影响(Hedges'g = 0.06),研究内和研究间异质性均为中等和低。抑郁症严重程度分析(14项研究- 2296名受试者- 116项影响)显示无效效应大小(Fisher's Z = 0.05),研究内部和研究之间没有中度异质性。两项荟萃分析均发现不对称。调节分析显示,抑郁严重程度、甲基化技术、单cpg位点、评估的细胞类型、年龄和女性比例没有显著影响。这项全面的综述为5-HTT启动子甲基化与抑郁症状之间复杂的相互作用提供了见解。此外,它为未来的研究工作提供了经过深思熟虑的建议,并描述了甲基化研究报告的指导方针。
Exploring the association between serotonin transporter promoter region methylation levels and depressive symptoms: a systematic review and multi-level meta-analysis.
Depressive disorders result from complex interactions among genetic, epigenetic, and environmental factors. DNA methylation, a key epigenetic mechanism, is crucial in understanding depressive symptoms development. The serotonin transporter gene (5-HTT) and its polymorphisms, like 5-HTTLPR, have been extensively studied in relation to depression, yet conflicting findings regarding the association between 5-HTT promoter methylation and depressive symptoms persist, largely due to methodological differences. Thus, this systematic review and meta-analysis aims to assess (1) 5-HTT promoter methylation levels between depressed and non-depressed conditions and (2) the association between 5-HTT methylation and depressive symptoms severity. We searched PubMed, Google Scholar, and Web of Science from inception to January 15th, 2025 (PROSPERO: CRD42023355414) and performed two independent multi-level meta-analyses to answer our aims. Twenty-four trials were included in the systematic review. All reported effects carried potential for bias. The meta-analysis for depression occurrence (12 studies - 2028 subjects - 127 effects) indicated no significant effect (Hedges'g = 0.06) with moderate within- and low between-study heterogeneity. The depression severity analysis (14 studies - 2296 subjects - 116 effects) revealed a null effect size (Fisher's Z = 0.05), with no within- and moderate between-study heterogeneity. Asymmetry was detected for both meta-analyses. Moderator analyses demonstrated no significant effects of depression severity, methylation techniques, single-CpG sites, cell types assessed, age, and female percentage. This comprehensive review provides insights into the intricate interplay between 5-HTT promoter methylation and depressive symptoms. Furthermore, it offers well-considered recommendations for future research endeavors and delineates guidelines for reporting methylation research.
期刊介绍:
Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.