Updated

Researchers at the Perelman School of Medicine at the University of Pennsylvania reported in Science Advances that TRF2, a protein long known for protecting chromosome ends, also helps muscle stem cells keep their identity and regenerate injured muscle in mice. When TRF2 was removed from these cells, the cells stayed alive but lost the molecular identity needed for repair, and injured muscles filled with fat and scar tissue instead of healthy muscle. Over time the population of functional muscle stem cells declined, and the mice became increasingly unable to repair damaged muscle. In a mouse model of Duchenne muscular dystrophy, removing TRF2 from muscle stem cells caused muscle degeneration to progress much faster and shortened the affected mice's survival. Senior author Foteini Mourkioti, an associate professor of Orthopedic Surgery at Penn Medicine, said the findings change how scientists think about TRF2's role in these cells. The article says the results do not yet establish a new treatment, but they identify a mechanism that could eventually be targeted to preserve muscle stem cell function. The researchers also suggested the work may help explain why skeletal muscle repairs itself so well while muscle-origin cancers are relatively uncommon.