Regenerative medicine could hold the keys to rejuvenating older muscles, and research supporting that will be featured at the Mayo Clinic Symposium on Regenerative Medicine and Surgery. Preclinical research by Helen Blau, Ph.D., Stanford University School of Medicine, discovered a protein that triggers muscle loss and a way to block it to restore youthful muscle strength. Dr. Blau, director of the Baxter Laboratory for Stem Cell Biology at Stanford University School of Medicine, will present her research in a virtual keynote speech.
"We identified the prostaglandin degrading enzyme 15-PGDH as a driver of muscle atrophy. Increasing levels of this enzyme in young mice induced muscle loss, and blocking this protein unleashed a hormone that overcame muscle wasting associated with aging," says Dr. Blau. "A major advantage of our approach is that it rejuvenated muscles by restoring the hormone prostaglandin E2 to physiological levels characteristic of young muscles."
The Mayo Clinic Symposium on Regenerative Medicine and Surgery will be held Nov. 4–7 at the JW Marriott Desert Resort and Spa in Phoenix. Register for the symposium, which will offer in-person and online sessions. Attendees can earn 15.75 continuing medical education credits.
Mayo Clinic's Center for Regenerative Medicine is sponsoring the symposium to advance its strategic goal of preparing future physicians and scientists to deliver new regenerative therapies that address unmet patient needs.
A common problem with no easy solutions
Muscles lose 10% to 15% of their size and strength every year after age 50, particularly in those who are inactive. This condition, known as sarcopenia, rapidly progresses in people over 65 who may lose as much as 50% to 80% of their lower body strength over time. That loss can lead to mobility problems, falls and loss of independence.
With no approved treatments for sarcopenia, chronic muscle loss exacts a huge toll on the quality of life and ultimately on society.
Dr. Blau's team not only identified accumulation of 15-PGDH as a driver of muscle weakness with aging in mice but also found it acted as a pivotal regulator of muscle function. Blocking this protein with a small molecule preserved the hormone-like substance of prostaglandin E2. That stimulated muscle stem cells to repair tissue loss and augmented mitochondrial function in mature muscle fibers to counter weakness in mice with sarcopenia. The research team documented a dramatic increase in muscle mass and strength within one month of treatment and observed that old mice were able to run for longer periods of time on treadmills.
This early research lays the foundation for new therapeutic strategies for reversing age-related muscle loss that so far have eluded medical science.
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