513 research outputs found
Epigenetic aging signatures in mice livers are slowed by dwarfism, calorie restriction and rapamycin treatment
Background: Global but predictable changes impact the DNA methylome as we age, acting as a type of molecular
clock. This clock can be hastened by conditions that decrease lifespan, raising the question of whether it can also
be slowed, for example, by conditions that increase lifespan. Mice are particularly appealing organisms for studies of
mammalian aging; however, epigenetic clocks have thus far been formulated only in humans.
Results: We first examined whether mice and humans experience similar patterns of change in the methylome with
age. We found moderate conservation of CpG sites for which methylation is altered with age, with both species
showing an increase in methylome disorder during aging. Based on this analysis, we formulated an epigenetic-aging
model in mice using the liver methylomes of 107 mice from 0.2 to 26.0 months old. To examine whether epigenetic
aging signatures are slowed by longevity-promoting interventions, we analyzed 28 additional methylomes from mice
subjected to lifespan-extending conditions, including Prop1df/df dwarfism, calorie restriction or dietary rapamycin. We
found that mice treated with these lifespan-extending interventions were significantly younger in epigenetic age than
their untreated, wild-type age-matched controls.
Conclusions: This study shows that lifespan-extending conditions can slow molecular changes associated with an
epigenetic clock in mice livers
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