Changes in epigenetic DNA methylation are the most promising predictor of biological age and lifespan in humans, but whether methylation changes affect ageing is unresolved. Here, we discuss converging data, which indicate that one mode by which aberrant DNA methylation can affect ageing is via CCAAT/enhancer binding protein beta (C/EBPβ). This basic leucine-zipper (bZIP) transcription factor is controlled by the lifespan regulator mechanistic/mammalian target of rapamycin complex 1 (mTORC1) and plays an important role in energy homeostasis and adipose tissue differentiation. Emerging evidence indicates that access of C/EBPβ proteins to cognate binding sites is regulated by DNA demethylation via ten-eleven translocation (TET) methylcytosine dioxygenases and their adaptor proteins growth arrest and DNA damage-inducible protein 45 alpha (GADD45α) and inhibitor of growth 1 (ING1). We discuss the emerging causal nexus between C/EBPβ, energy metabolism, and DNA demethylation in organismal ageing.

中文翻译：

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C /EBPβ和表观遗传DNA甲基化在衰老中的新兴作用。

表观遗传DNA甲基化的变化是人类生物学年龄和寿命的最有希望的预测指标，但是甲基化变化是否会影响衰老尚无定论。在这里，我们讨论会聚的数据，这表明异常DNA甲基化会影响衰老的一种模式是通过CCAAT /增强子结合蛋白β（C /EBPβ）。该基本的亮氨酸拉链（bZIP）转录因子受雷帕霉素复合物1（mTORC1）的寿命调节机制/哺乳动物靶标控制，并且在能量稳态和脂肪组织分化中起重要作用。新兴证据表明，C /EBPβ蛋白进入同源结合位点受DNA脱甲基作用的调控，该脱甲基作用是通过十一个11易位（TET）甲基胞嘧啶双加氧酶及其衔接蛋白的生长停滞和DNA损伤诱导蛋白45 alpha（GADD45α）以及生长抑制剂来实现的。 1（ING1）。我们讨论了有机衰老过程中C /EBPβ，能量代谢和DNA脱甲基之间出现的因果关系。