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首页> 外文期刊>Translational Stroke Research >Epigenetics and the Environment: In Search of the “Toleroasome” Vital to Execution of Ischemic Preconditioning
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Epigenetics and the Environment: In Search of the “Toleroasome” Vital to Execution of Ischemic Preconditioning

机译：表观遗传学与环境：寻找对缺血预处理至关重要的“耐受性”

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Activation and repression of gene expression are key features of ischemic tolerance. Converging lines of inquiry from several groups suggests that epigenetic proteins may transduce sublethal stresses, including bioenergetic or oxidative stress into durable (2–3 days) changes in gene expression that mediate ischemic tolerance. Here we discuss the potential mechanisms by which changes in cell state (e.g., ATP, NAD+, and oxygen) can modify specific targets including polycomb complexes, jumonji domain histone demethylases, and zinc and NAD-dependent histone decetylases and thus trigger an adaptive program. A major unanswered question is whether these proteins work in parallel or convergently as part of a “tolerosome” (tolero is the Latin word for tolerance), a multiprotein complex recruited to promoters or enhancers of specific genes, to mediate preconditioning. Whatever the case may be, epigenetic proteins are fertile targets for the treatment of stroke.
机译：基因表达的激活和抑制是缺血耐受的关键特征。几组研究的趋同线表明，表观遗传蛋白可能将亚致死应激（包括生物能或氧化应激）转化为介导缺血耐受的基因表达的持久性（2-3天）变化。在这里，我们讨论了细胞状态变化（例如ATP，NAD +和氧气）可以修饰特定靶标的潜在机制，包括多梳复合物，jumonji域组蛋白脱甲基酶以及锌和NAD依赖性组蛋白癸二酸酯，从而触发了适应性程序。一个主要的尚未解决的问题是这些蛋白质是作为“耐受体”（tolerosome）（耐受性的拉丁词，耐受性）的一部分并行或聚合起作用的，这种多蛋白复合体被募集到特定基因的启动子或增强子，以介导预处理。无论哪种情况，表观遗传蛋白都是治疗中风的可育靶标。

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