Aging Muscles Reveal Surprising Stem Cell Secrets

UCLA study uncovers how a protein called NDRG1 slows muscle repair but enhances stem cell survival in older adults

Apr. 10, 2026 at 5:56pm

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A highly detailed, translucent X-ray photograph revealing the internal structure of aged muscle tissue, with glowing, ghostly lines highlighting the NDRG1 protein and its role in the interplay between muscle stem cell activation and survival.An X-ray view into the complex molecular mechanisms underlying age-related muscle decline, where a key protein called NDRG1 plays a dual role in slowing repair but enhancing stem cell survival.Los Angeles Today

A new study from researchers at UCLA has uncovered an unexpected reason why aging muscles heal more slowly. The study found that a protein called NDRG1 accumulates in muscle stem cells as people get older, acting as a 'cellular brake' that suppresses the cells' ability to quickly activate and repair damaged tissue. However, this same protein also helps the aged stem cells survive longer, suggesting aging may involve complex trade-offs between function and resilience.

Why it matters

Understanding the molecular mechanisms behind age-related muscle decline is crucial for developing therapies that can restore youthful regenerative abilities without depleting the stem cell pool over time. This research challenges the conventional view of aging as purely detrimental, suggesting some changes may actually be protective adaptations.

The details

The study, published in the journal Science, revealed that NDRG1 levels increase dramatically with age, reaching 3.5 times higher in old muscle stem cells compared to young ones. This protein acts as a 'cellular brake', suppressing a key signaling pathway called mTOR that normally promotes cell activation and growth. When the researchers blocked NDRG1's activity in aged mice, the muscle stem cells behaved like young cells again, reactivating quickly and accelerating muscle repair after injury. However, this rejuvenation came at a cost - without NDRG1's protective effects, fewer muscle stem cells survived over time, limiting the tissue's ability to regenerate after repeated injuries.

  • The study was published in the journal Science on April 10, 2026.

The players

Dr. Thomas Rando

The senior author of the study and a professor at UCLA.

Jengmin Kang

A postdoctoral scholar and lead author of the study.

Daniel Benjamin

A postdoctoral scholar and co-lead author of the study.

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What they’re saying

“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. This gives us a completely different lens for understanding why tissues decline with age.”

— Dr. Thomas Rando, Senior author of the study

“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, but they're not good for the long term. 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

What’s next

The research team will continue investigating what controls the balance between stem cell survival and function at the molecular level, with the goal of developing therapies that can restore youthful regenerative abilities without depleting the stem cell pool over time.

The takeaway

This study challenges the conventional view of aging as purely detrimental, suggesting that some age-related changes in muscle stem cells may actually be protective adaptations. Understanding these complex trade-offs between function and resilience is crucial for developing effective therapies to combat age-related muscle decline.