创伤后应激障碍发病机制的表观遗传学和基因组学机制(综述)

А.Г. Фаустова, И. Ю. Юров
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引用次数: 0

摘要

背景:创伤后应激障碍是基因-环境相互作用最突出的例子之一。心理创伤是主要的病因,但不是唯一的病因。在过去的20年里,已经积累了足够的数据来证实遗传成分在所谓的“易感表型”形成中的作用。表观遗传修饰被认为是环境(创伤)暴露引发基因表达和基因组稳定性变化的一种机制,可导致特定症状。本研究的目的:总结和比较创伤后应激障碍基因组调控表观遗传机制的主要研究成果。材料与方法:对已发表的创伤后应激障碍表观遗传标记研究进行理论分析。PubMed数据库是在上述上下文中浏览的。结果:过去几十年发表的研究有一些共同的特点(依赖于通过自我报告法获得的创伤性事件的回顾性数据;使用可用的组织进行分析;采用回顾性横断面设计)。研究的系统分类学是基于两种主要方法(候选基因的搜索和研究;全基因组或表观基因组关联的方法)和DNA甲基化,组蛋白翻译后修饰和染色质结构组织的分析。创伤后应激障碍的发病机制也在细胞基因组假说(基因组不稳定水平的变化调节行为)的背景下得到解释。综述了创伤后应激障碍发病机制的表观遗传机制研究的局限性和前景。结论:表观遗传和基因组分析创伤后应激障碍的分子基础提供Обзор审查Научныерезультатыбиомедицинскихисследований。[2]李晓明。生物医学研究进展。2022:8(1):15-35 .以创伤性事件为表现的基因型与环境相互作用的最全面理解方法。表观遗传修饰和基因组不稳定性的研究可能是可逆的,将有助于改善对经历过创伤事件的个体的预防和提供临床和心理援助。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Epigenetic and genomic mechanisms in the pathogenesis of posttraumatic stress disorder (review)
Background: Posttraumatic stress disorder is one of the most prominent examples of gene-environment interactions. Psychological traumatization is a dominant, but not the only etiological factor. Over the past 20 years, sufficient data have been accumulated to confirm the role of the hereditary component in the formation of the so-called "vulnerable phenotype”. Epigenetic modifications are considered as a mechanism for environmental (traumatic) exposure provoking changes in gene expression and genome stability, which can lead to specific symptoms. The aim of the study: To summarize and to compare the essential results of studies of epigenetic mechanisms of genome regulation in posttraumatic stress disorder. Materials and methods: A theoretical analysis of the published studies dedicated to epigenetic markers of posttraumatic stress disorder was carried out. The PubMed database was browsed in the aforementioned context. Results: The studies published during the last decades have a number of common characteristics (reliance on retrospective data about a traumatic event obtained by the self-report method; use of available tissues for analysis; use of a retrospective cross-sectional design). The systematics of research is based on both the dominant methodology (search and study of candidate genes; methods of whole-genome or epigenome associations) and the analysis of DNA methylation, posttranslational modifications of histones, and chromatin structural organization. The pathogenesis of posttraumatic stress disorder is also explained in the context of cytogenomic hypothesis (changes in genome instability levels modulate behavior). The limitations and prospects of studying epigenetic mechanisms in the pathogenesis of posttraumatic stress disorder are outlined. Conclusion: Epigenetic and genomic analyses of the molecular basis of PTSD offer the Обзор Review Научные результаты биомедицинских исследований. 2022;8(1):15-35 Research Results in Biomedicine. 2022:8(1):15-35 17 most holistic approach to understanding the interaction between genotype and environment presenting as a traumatic event. The study of epigenetic modifications and genome instability, which are potentially reversible, will contribute to the improvement of the prevention and the provision of clinical and psychological assistance to individuals who have experienced traumatic events.
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