Signaling from dysfunctional mitochondria induces a distinct type of senescence
Buck Institute faculty Judith Campisi, PhD, says age researchers need to stop thinking of cellular senescence, now accepted as an important driver of aging, as a single phenotype that stems from genotoxic stress. Research from her lab reveals that cellular senescence, a process whereby cells permanently lose the ability to divide, is also induced by signaling from dysfunctional mitochondria - and that the arrested cells secrete a distinctly different "stew" of biologically active factors in a process unrelated to the damaging free radicals that are created in mitochondria as part of oxygen metabolism. The results are published in Cell Metabolism.
"We don't yet know how much this process contributes to natural aging," said Campisi, adding that those studies are currently underway. "But we do think the findings are important in addressing mitochondrial diseases, and those age-related diseases, such as some forms of Parkinson's, which involve mitochondrial dysfunction."
Fat biopsies stained for senescence (blue).Left: Normal wild type mice, aged 8 months. Right: Mouse model of mitochondrial progeria Credit: Akos Gerencser, PhD, Buck Institute