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Targeting Huntington’s disease through histone deacetylases

机译：通过组蛋白脱乙酰基酶靶向亨廷顿氏病

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Huntington’s disease (HD) is a debilitating neurodegenerative condition with significant burdens on both patient and healthcare costs. Despite extensive research, treatment options for patients with this condition remain limited. Aberrant post-translational modification (PTM) of proteins is emerging as an important element in the pathogenesis of HD. These PTMs include acetylation, phosphorylation, methylation, sumoylation and ubiquitination. Several families of proteins are involved with the regulation of these PTMs. In this review, I discuss the current evidence linking aberrant PTMs and/or aberrant regulation of the cellular machinery regulating these PTMs to HD pathogenesis. Finally, I discuss the evidence suggesting that pharmacologically targeting one of these protein families the histone deacetylases may be of potential therapeutic benefit in the treatment of HD.
机译：亨廷顿舞蹈病（HD）是一种使人衰弱的神经退行性疾病，给患者和医疗保健费用带来沉重负担。尽管进行了广泛的研究，但针对这种情况的患者的治疗选择仍然有限。蛋白质异常的翻译后修饰（PTM）正在成为HD发病机理中的重要元素。这些PTM包括乙酰化，磷酸化，甲基化，磺酰化和泛素化。几个蛋白质家族与这些PTM的调控有关。在这篇综述中，我讨论了将异常PTM和/或调节这些PTM的细胞机械异常调控与HD发病机制联系起来的最新证据。最后，我讨论了证据表明，以药理作用针对这些蛋白家族之一的组蛋白脱乙酰基酶可能在HD的治疗中具有潜在的治疗益处。

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