A research team at Tongji University in Shanghai has designed a short peptide that frees SIRT1, an enzyme closely tied to ageing, from a protein that holds it back. In laboratory cells the peptide raised SIRT1 activity and reduced signs of senescence. The study was published in Aging Cell on 30 October.
The peptide has so far been tested only in cells. The related work on mice looked at the protein that restrains SIRT1, not at the peptide.
Why SIRT1 matters
SIRT1 is an enzyme that helps keep cells in good working order. Earlier laboratory work has linked higher SIRT1 activity with slower senescence, the worn-out state in which cells stop dividing.
Senescent cells build up with age and are a major focus of ageing research, which is why proteins that control SIRT1 attract so much interest.
A brake called USP25
The Tongji team found that another protein, USP25, binds to SIRT1 and modifies it in a way that dampens its activity. That pushes cells towards senescence.
Mice bred without USP25 showed fewer age-related changes and better overall physiology, which supported the idea that USP25 acts as a brake on healthy ageing.
A peptide that breaks the pairing
The researchers then designed a cell-penetrating peptide, pSirt1-4, that breaks up the pairing between USP25 and SIRT1. In cells it raised SIRT1 activity and reduced signs of senescence.
The idea is to release the brake on SIRT1 by interrupting the contact between the two proteins, rather than by changing either protein permanently.
How early this is
The peptide itself has only been tested at the cell stage. Whether it works in a living animal, how it would be delivered and whether it is safe over time are questions for later studies.