Examine genetic differences in centenarians that modify cellular senescence and how those insights guide translational geroscience strategies.
Key Takeaways
- Centenarian-linked SIRT6 variants increased endogenous SIRT6 abundance via weaker vimentin interaction
- Variants enhanced mono-ADP-ribosylation and reduced deacetylase activity while delaying cellular senescence
- AAV delivery of centenarian SIRT6 or fucoidan activation partially reversed genome instability in progeria fibroblasts