Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Aug 11;166(4):822-839.
doi: 10.1016/j.cell.2016.07.050.

Epigenetic Mechanisms of Longevity and Aging

Payel Sen  1 , Parisha P Shah  1 , Raffaella Nativio  1 , Shelley L Berger  2
Affiliations
Review

Epigenetic Mechanisms of Longevity and Aging

Payel Sen et al. Cell. .

Abstract

Aging is an inevitable outcome of life, characterized by progressive decline in tissue and organ function and increased risk of mortality. Accumulating evidence links aging to genetic and epigenetic alterations. Given the reversible nature of epigenetic mechanisms, these pathways provide promising avenues for therapeutics against age-related decline and disease. In this review, we provide a comprehensive overview of epigenetic studies from invertebrate organisms, vertebrate models, tissues, and in vitro systems. We establish links between common operative aging pathways and hallmark chromatin signatures that can be used to identify "druggable" targets to counter human aging and age-related disease.

PubMed Disclaimer

Figures

Figure 1
Figure 1. The epigenetic hallmarks of senescence and aging
Senescence and aging are characterized by (A) loss of histones, (B) imbalance of activating and repressive modifications, (C) transcriptional changes, (D) losses and gains in heterochromatin, (E) breakdown of nuclear lamina, (F) global hypomethylation and focal hypermethylation and (G) chromatin remodeling. These changes are heavily dictated by (H) environmental stimuli (I) and nutrient availability that in turn (J) alter intracellular metabolite concentrations.
See this image and copyright information in PMC

References

    1. Adams PD. Healing and hurting: molecular mechanisms, functions, and pathologies of cellular senescence. Mol Cell. 2009;36:2–14. - PubMed
    1. Armstrong VL, Rakoczy S, Rojanathammanee L, Brown-Borg HM. Expression of DNA methyltransferases is influenced by growth hormone in the long-living Ames dwarf mouse in vivo and in vitro. J Gerontol A Biol Sci Med Sci. 2014;69:923–933. - PMC - PubMed
    1. Bahar R, Hartmann CH, Rodriguez KA, Denny AD, Busuttil RA, Dolle ME, Calder RB, Chisholm GB, Pollock BH, Klein CA, et al. Increased cell-to-cell variation in gene expression in ageing mouse heart. Nature. 2006;441:1011–1014. - PubMed
    1. Baker DJ, Jeganathan KB, Cameron JD, Thompson M, Juneja S, Kopecka A, Kumar R, Jenkins RB, de Groen PC, Roche P, et al. BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice. Nat Genet. 2004;36:744–749. - PubMed
    1. Baker DJ, Wijshake T, Tchkonia T, LeBrasseur NK, Childs BG, van de Sluis B, Kirkland JL, van Deursen JM. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature. 2011;479:232–236. - PMC - PubMed

Publication types