A landmark study published in Nature Aging has uncovered a previously unknown mechanism that drives cellular senescence, opening new avenues for anti-aging therapeutics. Researchers at the Salk Institute identified a protein complex called SAGA-7 that acts as a master regulator of cellular aging processes.
The team found that when SAGA-7 levels decline — a natural consequence of aging — cells lose their ability to efficiently repair damaged DNA. This leads to an accumulation of genetic errors that eventually triggers senescence, the state in which cells stop dividing and begin releasing inflammatory compounds.
"This discovery fundamentally changes our understanding of why cells age," said Dr. Elena Marchetti, lead author of the study. "By targeting SAGA-7 pathways, we may be able to slow or even partially reverse aspects of cellular aging."
The research team demonstrated that restoring SAGA-7 levels in aged mice rejuvenated their immune systems and improved tissue repair capabilities. Clinical trials in humans are expected to begin within two years, focusing initially on age-related immune decline.
The findings have generated significant excitement in the longevity research community, with several biotech companies already expressing interest in developing SAGA-7-based therapeutics.