Circadian clocks: a possible strategy to fight aging
- Yasukazu Nakahata Ph.D., Department of Neurobiology and Behaviour, Graduate School of Biomedical Sciences, Nagasaki University Nagasaki, Japan
Scientific Coordinator: Gianluca Esposito
Our research goal is to reveal molecular mechanisms connecting circadian clocks and aging process and contribute to extend healthy aging. To address this goal, we have first investigated at cellular level. So far, we have found that cellular senescence, aging at cellular level, triggers altered circadian clocks with a prolonged period and delayed phase. We have also found that intracellular NAD+ amount decreases with cellular senescence, furthermore, the onset of cellular senescence delays when NAMPT, which is the rate-limiting enzyme in NAD+ salvage pathway, is overexpressed. Our previous study that circadian clock and NAD+ salvage pathway are mutually regulated via NAD+/SIRT1 axis prompted us to investigate whether the boost of NAD+ in senescent cells recover the alteration of circadian clock properties. The answer was “yes”, circadian period was shortened in NAD+-boosted senescent cells and even aged mice. Now we have been struggling to reveal molecular mechanisms of how NAD+ influences circadian clocks. We have also started to find out other molecules which recover the alteration of circadian clock properties in senescent cells to understand how circadian clock regulates aging process and contribute to extend healthy aging. In this seminar, I will introduce the basic knowledge of the circadian clock aging process, and their relationship based on our findings.