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本文引用的文献

1
Systemic effects of mitochondrial stress.线粒体应激的系统效应。
EMBO Rep. 2020 Jun 4;21(6):e50094. doi: 10.15252/embr.202050094. Epub 2020 May 24.
2
Uncoupling histone H3K4 trimethylation from developmental gene expression via an equilibrium of COMPASS, Polycomb and DNA methylation.通过 COMPASS、Polycomb 和 DNA 甲基化之间的平衡,将组蛋白 H3K4 三甲基化与发育基因表达解偶联。
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Developmental ROS individualizes organismal stress resistance and lifespan.发育过程中的活性氧会使生物体的应激抵抗能力和寿命产生个体差异。
Nature. 2019 Dec;576(7786):301-305. doi: 10.1038/s41586-019-1814-y. Epub 2019 Dec 4.
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The proteostasis network and its decline in ageing.蛋白质稳态网络及其在衰老过程中的衰退。
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ATM phosphorylation of the actin-binding protein drebrin controls oxidation stress-resistance in mammalian neurons and C. elegans.ATM 磷酸化肌动蛋白结合蛋白 drebrin 控制哺乳动物神经元和秀丽隐杆线虫的氧化应激抗性。
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N6-methyldeoxyadenine is a transgenerational epigenetic signal for mitochondrial stress adaptation.N6-甲基脱氧腺嘌呤是线粒体应激适应的跨代表观遗传信号。
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8
The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseases.线粒体未折叠蛋白反应和线粒体代谢:代谢性疾病的一个新视角。
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9
Unique patterns of trimethylation of histone H3 lysine 4 are prone to changes during aging in Caenorhabditis elegans somatic cells.组蛋白 H3 赖氨酸 4 的三甲基化在秀丽隐杆线虫体细胞衰老过程中容易发生变化。
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10
Activation of DAF-16/FOXO by reactive oxygen species contributes to longevity in long-lived mitochondrial mutants in Caenorhabditis elegans.活性氧激活 DAF-16/FOXO 有助于线虫中长寿的线粒体突变体的长寿。
PLoS Genet. 2018 Mar 9;14(3):e1007268. doi: 10.1371/journal.pgen.1007268. eCollection 2018 Mar.

塑造生命早期的长寿:发育中的 ROS 和 H3K4me3 设定生物钟。

Shaping longevity early in life: developmental ROS and H3K4me3 set the clock.

机构信息

Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, USA.

出版信息

Cell Cycle. 2021 Nov;20(22):2337-2347. doi: 10.1080/15384101.2021.1986317. Epub 2021 Oct 17.

DOI:10.1080/15384101.2021.1986317
PMID:34657571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8794500/
Abstract

Studies in have revealed that even a genetically identical population of animals exposed to the same environment displays a remarkable level of variability in individual lifespan. Stochasticity factors, occurring seemingly by chance or at random, are thought to account for a large part of this variability. Recent studies in our lab using now revealed that naturally occurring variations in the levels of reactive oxygen species experienced early in life contribute to the observed lifespan variability, and likely serve as stochasticity factors in aging. Here, we will highlight how developmental events can positively shape lifespan and stress responses via a redox-sensitive epigenetic regulator, and discuss the outstanding questions and future directions on the complex relationship between reactive oxygen species and aging.

摘要

研究表明,即使是暴露在相同环境中的遗传上完全相同的动物群体,其个体寿命也表现出显著的变异性。随机因素,似乎是偶然或随机发生的,被认为是这种变异性的很大一部分原因。我们实验室最近的研究使用 现在表明,生命早期经历的活性氧水平的自然变化导致了观察到的寿命变异性,并可能作为衰老过程中的随机性因素。在这里,我们将重点介绍发育事件如何通过一种氧化还原敏感的表观遗传调节剂积极塑造寿命和应激反应,并讨论活性氧与衰老之间复杂关系的悬而未决的问题和未来方向。