ITHACA, N.Y. — Cornell University researchers have identified a molecular mechanism that constrains skeletal muscle regeneration and myofiber repair, a finding that could lead to improved treatment for conditions such as muscular dystrophy and severe injury.

To repair muscle, muscle cells, or myocytes, fuse to one another. But the molecular pathways that signal this cell-to-cell fusion have remained poorly defined.

“We don’t fully understand how muscle regeneration occurs after injury or during aging,” said Daniel Berry, the Andre Bensadoun, Ph.D. ’60 Associate Professor in the College of Human Ecology at Cornell.

The team, led by Berry, found that platelet-derived growth factor receptor beta (PDGFRb), a receptor protein located in cell membranes, is a key modulator of myocyte function in adult muscle cells. They published their findings Feb. 16 in the Journal of Clinical Investigation. The co-first authors are Siwen Xue, a doctoral student in molecular nutrition, and Abigail Benvie, Ph.D. ’24, now a postdoctoral fellow at Yale University.