创伤后应激障碍的表观遗传学改变:分子标记的全面回顾。

Complex psychiatry Pub Date : 2024-11-18 eCollection Date: 2024-01-01 DOI:10.1159/000541822
Elizaveta Golubeva, Angelina Zeltser, Yana Zorkina, Aleksandra Ochneva, Anna Tsurina, Denis Andreyuk, Georgiy Kostyuk, Anna Morozova
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引用次数: 0

摘要

背景:创伤后应激障碍(PTSD创伤后应激障碍(PTSD)可能发生在创伤事件之后。创伤后应激障碍的特征是噩梦、闪回和回避压力源。目前,2%-8%的人患有这种疾病,军人尤其易感。研究表明,环境压力可诱发各种表观遗传变化,从而形成创伤后应激障碍的表型。尽管表观遗传因素对创伤后应激障碍症状和易感性有重大影响,但文献中并未对其进行广泛讨论。本综述重点描述了创伤后应激障碍的表观遗传机制,尤其是DNA甲基化、染色质调控和非编码RNA。摘要:文章收录了2013年至2023年发表的相关研究,排除了非英语研究或数据不充分的研究。这篇综述调查了与创伤后应激障碍有关的基因甲基化变化,包括与下丘脑-垂体-肾上腺轴、脑源性神经营养因子、神经递质和免疫系统功能有关的基因甲基化变化,以及组蛋白和调控性非编码RNA的作用:表观遗传学的改变在创伤后应激障碍的易感性、症状学和长期结果的形成过程中起着至关重要的作用,凸显了其作为重要标记和治疗靶点的潜力。了解这些改变有助于制定临床策略,更好地预测、预防和治疗创伤后应激障碍。然而,还需要进一步开展大规模的纵向研究,以确定表观遗传变化与创伤后应激障碍发病之间的时间关系,并对其他潜在的表观遗传机制进行分类。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Epigenetic Alterations in Post-Traumatic Stress Disorder: Comprehensive Review of Molecular Markers.

Background: Post-traumatic stress disorder (PTSD) can occur after a traumatic event. PTSD is characterized by nightmares, flashbacks and avoidance of stressors. It currently affects 2-8% of the population, with military personnel particularly susceptible. Studies show that environmental stressors can induce various epigenetic changes that shape the PTSD phenotype. Despite the significant impact of epigenetic factors on PTSD symptoms and susceptibility, they have not been widely discussed in the literature. This review focuses on describing epigenetic mechanisms in PTSD, especially DNA methylation, chromatin regulation, and noncoding RNA.

Summary: The article includes relevant studies published from 2013 to 2023, excluding non-English-language studies or studies with insufficient data. This review investigated gene methylation changes in association with PTSD, including those related to the hypothalamic-pituitary-adrenal axis, brain-derived neurotrophic factor, neurotransmitters, and immune system functioning, as well as the role of histones and regulatory noncoding RNAs.

Key messages: Epigenetic alterations play a crucial role in shaping PTSD susceptibility, symptomatology, and long-term outcomes, highlighting their potential as important markers and therapeutic targets. Understanding these alterations can aid in developing clinical strategies to better predict, prevent, and treat PTSD. However, further large-scale longitudinal studies are needed to establish the temporal relationship between epigenetic changes and the onset of PTSD, as well as to classify other potential epigenetic mechanisms.

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