Epigenetic aging signatures in mice livers are slowed by dwarfism, calorie restriction and rapamycin treatment.
Level 5 - mechanism / opinion, no new human data
Animal research (preclinical mouse model)
PubMed 28351423 · doi:10.1186/s13059-017-1186-2
What was done
Researchers evaluated age-related DNA methylation patterns between mice and humans. Using liver methylomes from 107 mice aged 0.2 to 26.0 months, they constructed an epigenetic aging model for mice. They then tested whether longevity-promoting interventions decelerate this clock by analyzing 28 additional liver methylomes from mice subjected to Prop1 df/df dwarfism, calorie restriction, or dietary rapamycin compared to untreated, wild-type age-matched controls.
What was found
Mice and humans demonstrated moderate conservation of age-altered CpG sites, with both species exhibiting increased methylome disorder during aging. Mice receiving lifespan-extending interventions (dwarfism, calorie restriction, or rapamycin) were significantly younger in epigenetic age than untreated, age-matched controls. The abstract does not report specific numerical values, effect sizes, or p-values.
Why it matters
This study demonstrates that molecular epigenetic clocks operate in mice and can be decelerated by genetic, dietary, and pharmacological lifespan-extending interventions.
Limits
The study is restricted to mouse liver tissue, limiting direct inferences about other tissues or translation to humans. The intervention sample size was small (28 methylomes across three interventions and controls), and specific quantitative metrics of epigenetic age deceleration are not provided in the abstract.
Cited by
- supports Caloric restriction substantially slows epigenetic aging in mice, with longer duration producing progressively slower accumulation of epigenetic age.