Cell Metab. 2016 Oct 11;24(4):526-528. doi: 10.1016/j.cmet.2016.09.019.
Author information
- 1
- Novartis Professor, Koch Institute Affiliate and Director of the Paul F. Glenn Center for the Science of Aging Research, MIT, Cambridge, MA 02139, USA. Electronic address: leng@mit.edu.
Abstract
In this issue, Fang et al. (2016) show that both the DNA repair defect and mitochondrial dysfunction in ATM-/- cells or mice are mitigated by the anti-aging compound nicotinamide riboside or a SIRT1 activator. This broad suppression by activating the NAD+/SIRT1 axis may generally apply to diseases and aging maladies.
Comment on
- PMID:
- 27732834
- DOI:
- 10.1016/j.cmet.2016.09.019
- [Indexed for MEDLINE]