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Epigenetics, DNA damage, and aging
Carolina Soto-Palma, … , Christopher D. Faulk, Xiao Dong
Carolina Soto-Palma, … , Christopher D. Faulk, Xiao Dong
Published August 15, 2022
Citation Information: J Clin Invest. 2022;132(16):e158446. https://doi.org/10.1172/JCI158446.
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Review Series

Epigenetics, DNA damage, and aging

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Abstract

Over the course of a human lifespan, genome integrity erodes, leading to an increased abundance of several types of chromatin changes. The abundance of DNA lesions (chemical perturbations to nucleotides) increases with age, as does the number of genomic mutations and transcriptional disruptions caused by replication or transcription of those lesions, respectively. At the epigenetic level, precise DNA methylation patterns degrade, likely causing increasingly stochastic variations in gene expression. Similarly, the tight regulation of histone modifications begins to unravel. The genomic instability caused by these mechanisms allows transposon element reactivation and remobilization, further mutations, gene dysregulation, and cytoplasmic chromatin fragments. This cumulative genomic instability promotes cell signaling events that drive cell fate decisions and extracellular communications known to disrupt tissue homeostasis and regeneration. In this Review, we focus on age-related epigenetic changes and their interactions with age-related genomic changes that instigate these events.

Authors

Carolina Soto-Palma, Laura J. Niedernhofer, Christopher D. Faulk, Xiao Dong

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Figure 1

Epigenetics, DNA damage, and aging.

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Epigenetics, DNA damage, and aging.
Aging is determined, in part, by int...
Aging is determined, in part, by interrelated mechanisms that affect nuclear genome integrity: macromolecular damage to DNA and epigenetic alterations. DSBs, double-strand breaks; PTMs, posttranslational modifications; SSBs, single-strand breaks.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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