Aging Weakens Muscle Stem Cells' Regenerative Power

UCLA researchers discover a protein that protects aged muscle stem cells but slows their ability to repair tissue.

Jan. 30, 2026 at 12:47am

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A new UCLA study conducted in mice reveals that stem cells in aged muscle accumulate higher levels of a protein called NDRG1 that slows their ability to activate and repair tissue, but helps the cells survive longer in the harsh environment of aging tissue. When scientists blocked NDRG1 in aged mice, muscle stem cells behaved like young cells again and accelerated repair after injury. However, fewer stem cells survived over time, impairing regeneration after repeated injuries.

Why it matters

Aging muscles heal more slowly after injury, a frustrating reality for many older adults. This study suggests that some molecular changes associated with aging may actually be protective adaptations rather than purely detrimental effects, providing a new lens for understanding why tissues decline with age.

The details

The research team compared muscle stem cells isolated from young and old mice and discovered that NDRG1 increased dramatically with age, reaching levels 3.5 times higher in old cells than in young cells. NDRG1 acts as a cellular brake, suppressing a key signaling pathway called mTOR that normally promotes cell activation and growth. When NDRG1 was blocked in aged mice, the muscle stem cells immediately behaved like young cells again, reactivating quickly and accelerating muscle repair after injury. However, this rejuvenation came at a cost, as fewer muscle stem cells survived over time, limiting the muscle tissue's ability to regenerate after repeated injuries.

  • The research team studied muscle stem cells from young and aged mice both in laboratory dishes and in living tissues.

The players

Dr. Thomas Rando

Senior author of the study, director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, and professor of neurology at the David Geffen School of Medicine at UCLA.

Jengmin Kang

Postdoctoral scholar and lead author of the study.

Daniel Benjamin

Postdoctoral scholar and lead author of the study.

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What they’re saying

“This has led us to a new way of thinking about aging. It's counterintuitive, but the stem cells that make it through aging may actually be the least functional ones. They survive not because they're the best at their job, but because they're the best at surviving. That gives us a completely different lens for understanding why tissues decline with age.”

— Dr. Thomas Rando, Senior author of the study (Mirage News)

“Think of it like a marathon runner versus a sprinter. The stem cells in young animals are hyper-functioning — really good at what they do, namely sprinting, but they're not good for the long term. They can make it through the 100-yard dash, but they can't make it even halfway through the marathon. By contrast, aged stem cells are like marathon runners — slower to respond, but better equipped for the long haul. However, what makes them so proficient over long distances is exactly what renders them poor at sprinting.”

— Dr. Thomas Rando, Senior author of the study (Mirage News)

What’s next

The research team will continue investigating what controls the balance between survival and function of muscle stem cells at the molecular level.

The takeaway

This study suggests that some age-related changes that appear detrimental, like slower tissue repair, may actually be necessary compromises that prevent the complete depletion of the stem cell pool. Future therapies will need to balance both rapid repair capacity and long-term cellular survival to effectively combat age-related decline.