Muscle stem cells gain resilience but lose regenerative power with age

A UCLA study in mice found that aging muscle stem cells accumulate the protein NDRG1, which slows their activation and delays repair but enhances cell survival; blocking NDRG1 restored rapid repair yet reduced long-term stem cell survival.

Researchers at UCLA report that muscle stem cells in aged mice accumulate much higher levels of the protein NDRG1. That increase slows the cells’ ability to activate and repair muscle after injury, while also helping the cells survive in the stressed environment of aging tissue. The results, published in Science, led the authors to describe a form of "cellular survivorship bias" that leaves a slower but more resilient stem cell population. This finding frames some age-related molecular changes as protective adaptations rather than solely harmful effects. Key facts: - NDRG1 levels were about 3.5 times higher in muscle stem cells from old mice compared with young mice. - NDRG1 suppresses mTOR signaling, which reduces stem cell activation and delays rapid tissue repair. - Blocking NDRG1 in aged mice made the stem cells reactivate quickly and accelerated muscle repair after a single injury. - Removing NDRG1’s protective effect led to fewer surviving stem cells over time, limiting regeneration after repeated injuries. Summary: The study suggests that some age-related changes trade faster repair for long-term cell survival, helping to conserve the stem cell pool. The research team will continue investigating molecular controls of this balance; specific clinical implications are undetermined at this time.