Scientists at the University of California, Irvine’s School of Pharmacy & Pharmaceutical Sciences have identified a cellular mechanism that helps muscle stem cells repair damaged tissue. The research, published in Nature Metabolism, may offer new ways to address muscle loss related to aging, injury, and the use of weight-loss drugs.
The study found that after muscle stress or injury, stem cells slow their energy production and reroute glucose from being used as fuel to generating antioxidants. These antioxidants help reduce inflammation during the early stages of recovery. Once repairs are completed, the cells resume energy production and begin forming new muscle fibers.
“Muscle metabolism isn’t simply about fueling growth; it’s about strategic recovery,” said Lauren Albrecht, UC Irvine assistant professor of pharmaceutical sciences and the study’s corresponding author. “We found that muscle stem cells actively change how they use nutrients to protect themselves first, then rebuild. That metabolic timing is critical.”
Researchers discovered that an enzyme called PFKM plays a central role in this process by regulating how glucose is processed within cells. During initial repair phases, PFKM levels drop to create a pause in metabolism; when levels rise again, muscle building resumes.
The team also showed that providing certain metabolic building blocks—nutrients typically produced later in recovery—could speed up the shift from repair mode to growth mode in laboratory models.
“With the rapid rise of GLP-1 therapies and an aging population, preserving muscle mass has become a major health priority,” Albrecht said. “Our work identifies a metabolic checkpoint that could one day be targeted to help people recover muscle more effectively.”
The research involved advanced imaging techniques and analysis of human muscle data with participation from UCLA and Yale University scientists. Funding came from several organizations including the National Institutes of Health and the Alfred P. Sloan Foundation.
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