Researchers from the University of Glasgow in Scotland collaborated with colleagues at the Mayo Clinic in Minnesota to uncover a fresh mechanism behind aging. Their findings appear in the scientific journal Nature.
The team explored what drives inflammatory processes in older and damaged cells and proposed a strategy to interrupt this cycle. They observed that aging and certain cancer therapies can cause mitochondria, the tiny organelles that convert food into usable energy, to lose their tight seal and release DNA into the cell. This release triggers inflammation, which in turn accelerates the aging process.
“The research reveals an unexpected connection between mitochondrial changes and inflammatory responses in aged cells. When mitochondrial permeability increases, it promotes inflammation in old and damaged cells, opening new paths for research and potential therapies for aging and cancer,” stated Professor Stephen Tate, who led the study.
Earlier work hinted at methods to slow aging in animal models, but this study provides a clearer link between cellular energy hubs and inflammatory aging. Researchers emphasize that understanding this relationship could guide the development of treatments that mitigate age-related inflammation and improve healthspan in humans. [Citation: Nature journal, study by University of Glasgow and Mayo Clinic collaboration]