Researchers at the University of California, Los Angeles, have identified a key reason why muscle repair slows with age. In older muscle stem cells, a protein called NDRG1 accumulates and acts as a brake on rapid regeneration, according to a study published in the journal Science.

Understanding the Role of NDRG1

The finding reveals a biological trade-off: while NDRG1 slows activation and repair after injury, it enhances the cells’ long-term survival in the stressful environment of aging tissue. Blocking the protein restored youthful repair speed in aged mice but reduced stem cell numbers over time, impairing recovery from repeated injuries.

Researchers led by postdoctoral scholars Jengmin Kang and Daniel Benjamin compared muscle stem cells from young and old mice. They found NDRG1 levels rose dramatically with age, reaching concentrations 3.5 times higher in older cells.

Implications for Aging and Tissue Repair

NDRG1 suppresses the mTOR signaling pathway, which normally drives cell activation and growth. In experiments with mice aged to the human equivalent of about 75 years, blocking NDRG1 activity allowed older stem cells to activate more quickly and improve muscle repair after injury.

According to Dr. Thomas Rando, senior author of the study and director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, “It’s counterintuitive, but the stem cells that make it through aging may actually be the least functional ones. They survive not because they’re the best at their job, but because they’re the best at surviving.”

Original reporting: The Dallas Express — read the source article.