Histone Acetylation and Methylation Underlie Oligodendroglial and Myelin Susceptibility in Schizophrenia.

Histone Acetylation and Methylation Underlie Oligodendroglial and Myelin Susceptibility in Schizophrenia.
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DOI:
10.3389/fncel.2022.823708
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发表时间:
2022
影响因子:
5.3
通讯作者:
Chen X
Chen X
中科院分区:
医学2区
文献类型:
--
作者:
Li M;Xiao L;Chen X

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精神分裂症是一种复杂的神经精神疾病,受遗传和表观遗传因素的影响。除了神经元功能障碍外,少突胶质异常也有助于疾病的发病机制,其特征是少突胶质细胞和髓鞘相关基因的强烈失调。越来越多的证据表明,组蛋白修饰在对少突胶质细胞分化和髓鞘形成至关重要的基因的转录调控中起着重要作用。具体来说,组蛋白乙酰化和甲基化是精神分裂症大脑中两种公认的组蛋白修饰异常。在这篇综述中,我们将描述精神分裂症患者组蛋白乙酰化和甲基化的动态变化,这可能会协调和诱导少突胶质细胞的有害表观遗传记忆,并进一步导致少突胶质细胞和髓鞘缺陷。少突胶质细胞中组蛋白修饰状态的精确调节需要确保表观遗传标记的平衡,这可能会改变神经精神疾病白质病因学的治疗策略。
Schizophrenia is a complex neuropsychiatric disorder affected by both genetic and epigenetic factors. Except for neuronal dysfunction, oligodendroglial abnormalities also contribute to the disease pathogenesis, characterized by a robust dysregulation of oligodendrocyte and myelin related genes. Accumulating evidence shows that histone modifications play important roles in transcriptional regulation of the genes crucial for oligodendrocyte differentiation and myelination. Specifically, the histone acetylation and methylation were two well-recognized histone modification abnormalities in the schizophrenic brains. In this mini-review, we will describe the dynamic changes of histone acetylation and methylation in schizophrenia, which may coordinate and induce deleterious epigenetic memory in oligodendroglial cells, and further lead to oligodendrocyte and myelin deficits. Precise modulation of histone modification status in oligodendroglial cells needs to secure the balance of epigenetic marks, which may revise the therapeutic strategy for the white matter etiology of neuropsychiatric disorders.
脑可塑性,稳态和精神疾病中的少突胶质细胞。
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