Researchers at the University of Pennsylvania's Perelman School of Medicine discovered that the protein TRF2 is essential for maintaining muscle stem cell function and preventing tissue deterioration.
In mouse models, the absence of TRF2 caused injured muscle to transform into fat and scar tissue rather than regenerating, significantly accelerating the progression of Duchenne muscular dystrophy.
The study, published in Science Advances, suggests that TRF2 regulates muscle identity by locking onto G-quadruplex DNA shapes, offering potential new pathways for treating muscular dystrophy and cancer.