Histone modifying enzymes have vital roles in the growth and survival of both parasites and humans. Targeting the epigenome can be a new strategy for the treatment of parasitic diseases. Compounds modulating histone acetylation/deacetylation have recently been reported hampering Plasmodium, Schistosoma, Leishmania, and Trypanosoma infections. Beside new histone deacetylase inhibitors, PfGCN5 and bromodomain inhibitors have been recently described to inhibit Plasmodium proliferation. Sm histone deacetylase 8 and SmSIRT2, as well as Leishmania and Trypanosoma sirtuins (SIR2rps), seem to be the most reliable targets to effectively fight the related protozoan infections. The selectivity toward parasite over mammalian cells is still an open question, and significant optimization efforts of epidrugs are still required to improve potency/selectivity and decrease toxicity. Recent reports on the alteration of cellular signaling pathways provoked by parasite infection through changes in the host acetylation/deacetylation status at gene promoters may suggest novel therapeutic strategies to treat these diseases.

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针对寄生虫的组蛋白乙酰化/脱乙酰化：更新（2017-2020年）。

组蛋白修饰酶在寄生虫和人类的生长和存活中都起着至关重要的作用。靶向表观基因组可能是治疗寄生虫疾病的新策略。最近已经报道了调节组蛋白乙酰化/脱乙酰化的化合物阻碍了疟原虫，血吸虫，利什曼原虫和锥虫的感染。除了新的组蛋白脱乙酰基酶抑制剂外，最近还描述了PfGCN5和bromodomain抑制剂可抑制疟原虫的增殖。Sm组蛋白脱乙酰基酶8和SmSIRT2以及利什曼原虫和瑟氏锥虫（SIR2rps）似乎是有效对抗相关原生动物感染的最可靠目标。哺乳动物细胞对寄生虫的选择性仍然是一个悬而未决的问题，仍然需要大量的优化前体药物来提高效能/选择性并降低毒性。关于寄生虫感染通过基因启动子上宿主乙酰化/脱乙酰化状态的改变引起的细胞信号通路改变的最新报道可能提出了治疗这些疾病的新型治疗策略。