Mechanisms and interventions of epigenetic aging

IF 9 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Qingqing Chu , Yihang Li , Zeming Wu , Jing Qu , Guang-Hui Liu
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引用次数: 0

Abstract

Increasing evidence suggests that epigenetic dysregulation is both a hallmark and a potential driving force of aging. As a multifactorial, non-linear, and systemic biological process, aging likely results from a progressive imbalance in a complex epigenetic network involving DNA, histones, RNA, and non-coding sequences. These interconnected alterations collectively lead to core aging features such as genomic instability, heightened inflammation, and loss of cellular identity. In this review, we highlight the central role of epigenetic mechanisms across different dimensions in cellular, tissue, and organismal aging. Furthermore, we discuss potential intervention strategies designed to counteract these epigenetic alterations, indicating both their promise and the associated challenges.

Abstract Image

表观遗传衰老的机制及干预措施
越来越多的证据表明,表观遗传失调既是衰老的标志,也是潜在的驱动力。作为一个多因素、非线性和系统性的生物学过程,衰老可能是一个复杂的表观遗传网络(包括DNA、组蛋白、RNA和非编码序列)逐渐失衡的结果。这些相互关联的改变共同导致核心衰老特征,如基因组不稳定、炎症加剧和细胞身份丧失。在这篇综述中,我们强调了表观遗传机制在细胞、组织和有机体衰老中不同维度的核心作用。此外,我们讨论了旨在抵消这些表观遗传改变的潜在干预策略,指出了它们的前景和相关的挑战。
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来源期刊
Cell Chemical Biology
Cell Chemical Biology Biochemistry, Genetics and Molecular Biology-Molecular Medicine
CiteScore
14.70
自引率
2.30%
发文量
143
期刊介绍: Cell Chemical Biology, a Cell Press journal established in 1994 as Chemistry & Biology, focuses on publishing crucial advances in chemical biology research with broad appeal to our diverse community, spanning basic scientists to clinicians. Pioneering investigations at the chemistry-biology interface, the journal fosters collaboration between these disciplines. We encourage submissions providing significant conceptual advancements of broad interest across chemical, biological, clinical, and related fields. Particularly sought are articles utilizing chemical tools to perturb, visualize, and measure biological systems, offering unique insights into molecular mechanisms, disease biology, and therapeutics.
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