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Epigenetic mechanisms of neurodegeneration in Huntington's disease.亨廷顿病中神经退行性变的表观遗传机制。
Neurotherapeutics. 2013 Oct;10(4):664-76. doi: 10.1007/s13311-013-0206-5.
2
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3
Nucleolar dysfunction in Huntington's disease.亨廷顿舞蹈病中的核仁功能障碍。
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Epigenetic regulation in Huntington's disease.亨廷顿病的表观遗传调控。
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Epigenetic Mechanisms Involved in Huntington's Disease Pathogenesis.亨廷顿舞蹈病发病机制中的表观遗传机制
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Mechanisms of disease: Histone modifications in Huntington's disease.疾病机制：亨廷顿舞蹈症中的组蛋白修饰
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Mechanisms of neurodegeneration in Huntington's disease.亨廷顿舞蹈症中的神经退行性变机制。
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Epigenetic modifications as novel therapeutic targets for Huntington's disease.表观遗传学修饰作为亨廷顿病的新治疗靶点。
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Long non-coding RNAs in Huntington's disease neurodegeneration.亨廷顿病神经退行性变中的长非编码 RNA。
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Med Res Rev. 2025 May;45(3):985-1015. doi: 10.1002/med.22096. Epub 2025 Jan 6.
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MedComm (2020). 2024 Aug 4;5(8):e674. doi: 10.1002/mco2.674. eCollection 2024 Aug.
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Neuroinflammation and the role of epigenetic-based therapies for Huntington's disease management: the new paradigm.神经炎症与基于表观遗传的亨廷顿病治疗策略：新范例。
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Factors Influencing the Total Functional Capacity Score as a Critical Endpoint in Huntington's Disease Research.影响总功能能力评分作为亨廷顿舞蹈症研究关键终点的因素。
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Naïve Huntington's disease microglia mount a normal response to inflammatory stimuli but display a partially impaired development of innate immune tolerance that can be counteracted by ganglioside GM1.幼稚型亨廷顿病小胶质细胞对炎症刺激产生正常反应，但先天免疫耐受的发育部分受损，这种损伤可以通过神经节苷脂 GM1 来逆转。
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Role of DNMTs in the Brain.DNA甲基转移酶在大脑中的作用。
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Gene Alterations Induced by Glutamine (Q) Encoding CAG Repeats Associated with Neurodegeneration.谷氨酰胺（Q）编码 CAG 重复诱导的基因突变与神经退行性变有关。
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The emerging role of long non-coding RNAs, microRNAs, and an accelerated epigenetic age in Huntington's disease.长链非编码RNA、微小RNA的新作用以及亨廷顿舞蹈病中加速的表观遗传衰老
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Huntington's disease iPSC models-using human patient cells to understand the pathology caused by expanded CAG repeats.亨廷顿舞蹈症诱导多能干细胞模型——利用人类患者细胞来了解由CAG重复序列扩增所导致的病理状况。
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Posttranslational Modifications in Thyroid Cancer: Implications for Pathogenesis, Diagnosis, Classification, and Treatment.甲状腺癌中的翻译后修饰：对发病机制、诊断、分类和治疗的影响
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本文引用的文献

1
Epigenetic regulation of cholinergic receptor M1 (CHRM1) by histone H3K9me3 impairs Ca(2+) signaling in Huntington's disease.组蛋白 H3K9me3 对乙酰胆碱受体 M1 (CHRM1) 的表观遗传调控损害亨廷顿病中的 Ca(2+) 信号传导。
Acta Neuropathol. 2013 May;125(5):727-39. doi: 10.1007/s00401-013-1103-z. Epub 2013 Mar 2.
2
A novel method for detecting 7-methyl guanine reveals aberrant methylation levels in Huntington disease.一种检测 7-甲基鸟嘌呤的新方法揭示了亨廷顿病中异常的甲基化水平。
Anal Biochem. 2013 May 15;436(2):112-20. doi: 10.1016/j.ab.2013.01.035. Epub 2013 Feb 12.
3
Neurodegenerative disease: altered DNA methylation and RNA splicing could be key mechanisms in Huntington disease.神经退行性疾病：DNA甲基化和RNA剪接改变可能是亨廷顿病的关键机制。
Nat Rev Neurol. 2013 Mar;9(3):119. doi: 10.1038/nrneurol.2013.23. Epub 2013 Feb 12.
4
Increased 5-methylcytosine and decreased 5-hydroxymethylcytosine levels are associated with reduced striatal A2AR levels in Huntington's disease.甲基化胞嘧啶水平升高和羟甲基化胞嘧啶水平降低与亨廷顿病纹状体 A2AR 水平降低有关。
Neuromolecular Med. 2013 Jun;15(2):295-309. doi: 10.1007/s12017-013-8219-0. Epub 2013 Feb 6.
5
Extensive changes in DNA methylation are associated with expression of mutant huntingtin.广泛的 DNA 甲基化变化与突变 huntingtin 的表达有关。
Proc Natl Acad Sci U S A. 2013 Feb 5;110(6):2354-9. doi: 10.1073/pnas.1221292110. Epub 2013 Jan 22.
6
Selective histone deacetylase (HDAC) inhibition imparts beneficial effects in Huntington's disease mice: implications for the ubiquitin-proteasomal and autophagy systems.选择性组蛋白去乙酰化酶（HDAC）抑制在亨廷顿病小鼠中具有有益作用：对泛素-蛋白酶体和自噬系统的影响。
Hum Mol Genet. 2012 Dec 15;21(24):5280-93. doi: 10.1093/hmg/dds379. Epub 2012 Sep 10.
7
Single-stranded RNAs use RNAi to potently and allele-selectively inhibit mutant huntingtin expression.单链 RNA 通过 RNAi 强效且等位基因选择性地抑制突变型亨廷顿蛋白的表达。
Cell. 2012 Aug 31;150(5):895-908. doi: 10.1016/j.cell.2012.08.002.
8
Genome-wide histone acetylation is altered in a transgenic mouse model of Huntington's disease.亨廷顿病转基因小鼠模型中全基因组组蛋白乙酰化改变。
PLoS One. 2012;7(7):e41423. doi: 10.1371/journal.pone.0041423. Epub 2012 Jul 27.
9
Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease.组蛋白去乙酰化酶（HDAC）抑制剂靶向 HDAC3 和 HDAC1 可改善亨廷顿病模型系统中多聚谷氨酰胺引起的表型。
Neurobiol Dis. 2012 May;46(2):351-61. doi: 10.1016/j.nbd.2012.01.016.
10
Using non-coding small RNAs to develop therapies for Huntington's disease.利用非编码小 RNA 开发亨廷顿病的治疗方法。
Gene Ther. 2011 Dec;18(12):1139-49. doi: 10.1038/gt.2011.170.

亨廷顿病中神经退行性变的表观遗传机制。

Epigenetic mechanisms of neurodegeneration in Huntington's disease.

机构信息

Boston University Alzheimer's Disease Center and Department of Neurology, Boston University School of Medicine, Boston, MA, 02118, USA.

出版信息

Neurotherapeutics. 2013 Oct;10(4):664-76. doi: 10.1007/s13311-013-0206-5.

DOI:10.1007/s13311-013-0206-5
PMID:24006238
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3805871/
Abstract

Huntington's disease (HD) is an incurable and fatal hereditary neurodegenerative disorder of mid-life onset characterized by chorea, emotional distress, and progressive cognitive decline. HD is caused by an expansion of CAG repeats coding for glutamine (Q) in exon 1 of the huntingtin gene. Recent studies suggest that epigenetic modifications may play a key role in HD pathogenesis. Alterations of the epigenetic "histone code" lead to chromatin remodeling and deregulation of neuronal gene transcription that are prominently linked to HD pathogenesis. Furthermore, specific noncoding RNAs and microRNAs are associated with neuronal damage in HD. In this review, we discuss how DNA methylation, post-translational modifications of histone, and noncoding RNA function are affected and involved in HD pathogenesis. In addition, we summarize the therapeutic effects of histone deacetylase inhibitors and DNA binding drugs on epigenetic modifications and neuropathological sequelae in HD. Our understanding of the role of these epigenetic mechanisms may lead to the identification of novel biological markers and new therapeutic targets to treat HD.

摘要

亨廷顿病（HD）是一种无法治愈和致命的中年起病的遗传性神经退行性疾病，其特征为舞蹈病、情绪困扰和进行性认知衰退。HD 是由亨廷顿基因 1 号外显子中编码谷氨酸（Q）的 CAG 重复扩展引起的。最近的研究表明，表观遗传修饰可能在 HD 的发病机制中起关键作用。表观遗传“组蛋白密码”的改变导致染色质重塑和神经元基因转录的失调，这与 HD 的发病机制密切相关。此外，特定的非编码 RNA 和 microRNAs 与 HD 中的神经元损伤有关。在这篇综述中，我们讨论了 DNA 甲基化、组蛋白的翻译后修饰以及非编码 RNA 功能如何受到影响，并参与了 HD 的发病机制。此外，我们总结了组蛋白去乙酰化酶抑制剂和 DNA 结合药物对 HD 中表观遗传修饰和神经病理学后果的治疗作用。我们对这些表观遗传机制作用的理解可能会导致发现新的生物标志物和治疗 HD 的新靶点。