Duke-NUS names DEAF1 as the molecular switch behind muscle aging and how exercise lowers it
Researchers at Duke-NUS have named a molecular switch behind muscle aging: the gene DEAF1. It rises in older muscle and pushes mTORC1 into overactivity, disrupting protein turnover. Exercise lowers DEAF1 and restores the balance, giving the effect a concrete target. Source: PNAS,
Researchers at Duke-NUS Medical School have identified a specific gene that helps explain why exercise keeps aging muscle healthy. The gene, DEAF1, rises as muscle gets older. As its levels climb, it pushes a growth regulator called mTORC1 into overactivity, which interferes with the normal turnover of proteins inside muscle cells and accelerates decline. The team, working with Singapore General Hospital and Cardiff University, found that physical activity lowers DEAF1 and restores the balance between protein production and protein removal. That is the mechanism that keeps older muscle able to repair itself. The finding matters because it converts a well-known observation, that exercise slows muscle aging, into a specific molecular target that researchers can study directly. The study was published in July 2026 in the Proceedings of the National Academy of Sciences, as reported in coverage of the Duke-NUS work.