Researchers Uncover Molecular Mechanism Limiting Muscle Repair

Findings could lead to improved treatments for muscular dystrophy and severe injuries.

Published on Feb. 25, 2026

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Researchers at Cornell University's Division of Nutritional Sciences have identified a molecular mechanism that constrains skeletal muscle regeneration and myofiber repair. The team found that the receptor protein platelet-derived growth factor receptor beta (PDGFRb) serves as a key modulator of myocyte function in adult muscle cells, and that genetically deleting PDGFRb enhanced muscle regeneration and increased myofiber size, while activating PDGFRb impaired muscle repair.

Why it matters

This discovery represents a previously unrecognized function of PDGFRb and could lead to improved treatments for conditions like muscular dystrophy and severe muscle injuries, where enhancing muscle regeneration is critical.

The details

The researchers were initially studying the effects of a small molecule inhibitor related to the cancer drug imatinib on fat tissue, when they noticed changes in muscle function that prompted them to investigate the role of PDGFRb in muscle. Through in vitro and in vivo experiments, they found that genetic deletion of PDGFRb enhanced muscle regeneration and increased myofiber size, while PDGFRb activation impaired muscle repair. Further study indicated that treating muscle cells with the PDGFRb-inhibiting drug improved muscle development, suggesting the growth factor receptor serves as a checkpoint in muscle regeneration.

  • The findings were published on February 16, 2026 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.

The players

Daniel Berry

The Andre Bensadoun, Ph.D. '60 Associate Professor in the College of Human Ecology at Cornell University, who led the research team.

Siwen Xue

A doctoral student in molecular nutrition at Cornell University and co-first author of the study.

Abigail Benvie

A Ph.D. '24 graduate from Cornell University, now a postdoctoral fellow at Yale University, and co-first author of the study.

Anna Thalacker-Mercer

Formerly a researcher at Cornell University and now an associate professor at the University of Alabama, Birmingham, who collaborated with the research team to translate the findings from mouse models to human models.

Ben Cosgrove

An associate professor of biomedical engineering in Cornell Duffield Engineering, who contributed to the research.

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What they’re saying

“We don't fully understand how muscle regeneration occurs after injury or during aging.”

— Daniel Berry, The Andre Bensadoun, Ph.D. '60 Associate Professor in the College of Human Ecology (Mirage News)

“We started looking at muscle development and metabolism, and uncovered an unexpected role in regeneration. We found that muscle could recover faster when we deleted the receptor, and when we activated the receptor, recovery slowed down.”

— Daniel Berry, The Andre Bensadoun, Ph.D. '60 Associate Professor in the College of Human Ecology (Mirage News)

“The surprising finding was its role in regeneration. We think of tyrosine kinase receptors as drivers of cell growth and survival, not as determinants of cell fusion. That represents a previously unrecognized function.”

— Daniel Berry, The Andre Bensadoun, Ph.D. '60 Associate Professor in the College of Human Ecology (Mirage News)

What’s next

The research team is now studying muscle development during the embryonic stage and how that shapes muscle formation over an animal's lifetime, with the goal of designing strategies to preserve muscle during aging, disease, or rapid weight loss.

The takeaway

This discovery of PDGFRb's role as a checkpoint in muscle regeneration represents a significant advancement in understanding the molecular mechanisms underlying muscle repair, which could lead to new therapies for conditions where enhancing muscle regeneration is critical, such as muscular dystrophy and severe injuries.