Counteracting aged DNA methylation states to combat ageing and age-related diseases

https://doi.org/10.1016/j.mad.2022.111695Get rights and content
Under a Creative Commons license
open access

Highlights

  • Ageing alters genomic DNA methylation patterns towards pathogenic profiles.

  • Epigenetic clocks can track methylome ageing and related disease risks.

  • Epigenetic clocks offer new and unprecedented opportunities to develop strategies against epigenetic ageing.

  • Epigenetic ageing and ageing phenotypes can be counteracted in animal models.

  • Diet/lifestyle control is a promising epigenetic age-lowering strategy in humans.

Abstract

DNA methylation (DNAm) overwrites information about multiple extrinsic factors on the genome. Age is one of these factors. Age causes characteristic DNAm changes that are thought to be not only major drivers of normal ageing but also precursors to diseases, cancer being one of these. Although there is still much to learn about the relationship between ageing, age-related diseases and DNAm, we now know how to interpret some of the effects caused by age in the form of changes in methylation marks at specific loci. In fact, these changes form the basis of the so called “epigenetic clocks”, which translate the genomic methylation profile into an “epigenetic age”. Epigenetic age does not only estimate chronological age but can also predict the risk of chronic diseases and mortality. Epigenetic age is believed to be one of the most accurate metrics of biological age. Initial evidence has recently been gathered pointing to the possibility that the rate of epigenetic ageing can be slowed down or even reversed. In this review, we discuss some of the most relevant advances in this field. Expected outcome is that this approach can provide insights into how to preserve health and reduce the impact of ageing diseases in humans.

Keywords

Epigenetics
DNA methylation
Ageing
Disease
Epigenetic clock

Data availability

No data was used for the research described in the article.

Cited by (0)