Scientists discover how exercise reverses muscle aging — SkimNews
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- Duke-NUS Medical School researchers identified the DEAF1 gene as a regulator of age-related muscle decline, publishing the results in PNAS with collaborators from Singapore General Hospital and Cardiff University.
- As muscles age, rising DEAF1 levels drive excessive mTORC1 activity, causing damaged proteins to accumulate and disrupting the cycle of cellular maintenance — a breakdown tied to declining FOXO protein regulation.
- Exercise counteracts the cascade by activating proteins that reduce DEAF1, restoring the balance between protein production and cleanup so aging muscles can rebuild themselves.
- In fruit fly and mouse experiments, raising DEAF1 weakened muscles while reducing it restored strength, evidence the mechanism sits in an evolutionarily conserved pathway shared across species.
- First author Priscillia Choy Sze Mun framed DEAF1 reduction as "hitting the rewind button" on aging muscles, while lead author Asst Prof Tang Hong-Wen called the gene a therapy target for people unable to exercise due to surgery, illness, or cancer.
- The researchers cautioned a key limitation: when DEAF1 surges too high or FOXO activity drops too low, exercise alone may no longer fully reverse the damage, which could help explain why some older adults benefit more from physical activity than others.
Why it matters: DEAF1 gives drug developers a concrete molecular target for preserving muscle mass in older adults who cannot exercise — including post-surgical, chronically ill, and cancer patients — potentially extending the benefits typically gained from physical activity to a population that often cannot access them. Singapore's aging demographics make this translational research especially relevant to caregiver and healthcare-system strain.
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