When scientists removed NDRG1 in older mice, healing after injury improved quickly and visibly. Those gains came with a cost: the stem cells lost some long-term resilience and could be more vulnerable later. The study frames aging as a trade-off where the body may trade rapid recovery for cellular survival.
This finding matters because it shifts how we think about interventions for aging tissues. Therapies that boost repair could undermine durability, and approaches that strengthen resilience might slow recovery. Follow the link to see how this work could reshape strategies for healthier muscles, longer careers for stem cells, and what that means for human potential and inclusive access to future treatments.
A UCLA study in mice reveals that aging muscle stem cells accumulate a protein that slows repair but boosts survival. This protein, NDRG1, acts like a brake, preventing cells from activating quickly after injury. When researchers blocked it in older mice, muscle healing sped up dramatically — but stem cells became less resilient over time. The work suggests aging may reflect a survival trade-off rather than straightforward decline.
