Post-traumatic stress disorder (PTSD) is a mental disorder with complex etiology, which mostly occurs after severe traumatic events. The genesis and development of PTSD involves complex interactions between environmental triggers and genetic susceptibility, resulting in great individual differences. As a discipline investigating the changes in gene expression regulated by environment factors, the role of epigenetics in PTSD is attracting more and more attention in recent years. Histone modification, as one of the epigenetic mechanisms, plays an important role in the biological pathways for PTSD. Since histone modification can be regulated by a variety of enzymes, its flexible reversibility and elaborate regulation provides the possibility and convenience for the corresponding drug development. Therefore, in-depth exploration of the histone modification for the clinical treatment and drug development of PTSD is of great significance. Current studies on histone modification in PTSD mainly use animal models, with few clinical studies, focusing on histone H3 and H4 acetylation. In addition, consistent with previous findings, the changes in histone modification mostly occurred in prefrontal cortex, hippocampus, and amygdala, involved in the regulation of related pathways including the immune system, serotonin system, and the neuropeptide Y system. Current findings about histone modification in PTSD showed great heterogeneity, future studies should adopt more consistent and practical methods of analysis and reporting, to maximize study impact.

创伤后应激障碍是一种具有复杂病因学的精神疾病,多发生于个体受到重大创伤事件后。创伤后应激障碍的发生发展过程受到环境和遗传易感性的共同作用,存在着较大的个体差异;而表观遗传学作为一门研究多变环境因素调控基因表达的可遗传变化的学科,近年来在创伤后应激障碍的研究中受到越来越多的重视。表观遗传机制之一——组蛋白修饰机制在创伤后应激障碍的发生中起着重要作用,并且由于组蛋白修饰可以受到多种酶的调控,其灵活的可逆化和精细调控为相应的药物研发提供了可能性和便利。因此,深入探讨创伤后应激障碍的组蛋白修饰机制,对于相关疾病的临床治疗及药物研发具有十分重要的意义。当前创伤后应激障碍的组蛋白修饰研究主要使用动物模型,临床研究较少;组蛋白的类型则主要关注组蛋白H3和H4乙酰化;此外,同以往的研究结果一致,组蛋白修饰水平的变化主要发生在前额叶、海马体和杏仁核区域,参与免疫系统、血清素系统和神经肽Y能系统等相关通路的调节。当前PTSD组蛋白修饰的研究结果间还存在较大的异质性,未来的研究应采用更加一致和实用的分析和报道方法,以最大限度地发挥研究的影响。