DNA methylation patterns provide a robust molecular readout of biological age across mammalian tissues and species. Over the past decade, our laboratory has developed and validated multiple epigenetic clocks that predict chronological age, mortality risk, and physiologic decline. These clocks show that aging is an actively regulated epigenetic program that can be accelerated by disease and environmental stressors and can be slowed or reversed.

I will review the current landscape of epigenetic clocks and discuss what has been learnt about their mechanism. I will then present mechanistic studies in mice that illuminate how epigenetic aging can be modulated.

Finally, I will highlight translational efforts, including the development of blood-based epigenetic biomarkers for monitoring rejuvenation therapies in ongoing human clinical trials and the integration of epigenetic clocks with multi-omic aging atlases. These findings support the emerging view that aging is, at least in part, an epigenetic disease amenable to intervention, opening new therapeutic avenues for age-related conditions.