REVIEW: Aging Epigenetics: Accumulation of Errors or Realization of a Specific Program?

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V. V. Ashapkin^*, L. I. Kutueva, and B. F. Vanyushin

Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia; fax: + 7 (495) 939-3181; E-mail: ashapkin@genebee.msu.ru

^* To whom correspondence should be addressed.

Received July 6, 2015; Revision received July 13, 2015

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Aging in mammals is known to be accompanied by a progressive loss of methylated cytosines from DNA. This loss is tissue-specific to a certain extent and affects mainly repeated sequences, transposable elements, and intergenic genome parts. Age-dependent DNA hypomethylation is correlated with and perhaps partly caused by a diminished activity of DNA methyltransferases. Along with the global DNA demethylation during aging, hypermethylation of certain genes occurs. On the whole-genome scale, an age-dependent hypermethylation is typical for genes associated with promoter CG islands, whereas hypomethylation mostly affects CG-poor genes, besides the repeated sequences, transposable elements, and intergenic genome parts mentioned above. The methylation levels of certain CG sites display strict correlation to age and thus could be used as a molecular marker to predict biological age of cells, tissues, and organisms. Epigenetic cell reprogramming, such as induced pluripotent stem cell production, leads to complete resetting of their epigenetic age.

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KEY WORDS: epigenetics, aging, DNA methylation, epigenetic age, epigenetic reprogramming

DOI: 10.1134/S0006297915110024

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