Why do young tissues heal so effectively, while aging and diseased tissues lose their ability to regenerate?

Our laboratory studies this question using skeletal muscle as a model system. Muscle contains a remarkable population of stem cells that can rebuild damaged tissue after injury, yet this regenerative capacity declines during aging and is severely compromised in diseases such as muscular dystrophy. Aging and disease profoundly alter the tissue environment, changing the inflammatory, metabolic, and extracellular signals that muscle stem cells receive. We seek to understand how these environmental changes influence stem cell behavior and how they are interpreted through gene regulatory and epigenetic mechanisms to determine whether regeneration succeeds or fails. By combining stem cell biology, genomics, epigenetics, computational biology, and regenerative medicine, we investigate the mechanisms that control tissue repair and identify strategies to restore regenerative capacity when it is lost. Through studies in mouse models and human tissues, we aim to uncover the factors that determine regenerative competence and how they can be manipulated therapeutically.