Mitochondria's Role in Suppressing Inflammation in Aging Cells Revealed

Cells can enter a state called senescence, where they persist but no longer divide. These cells often secrete inflammatory molecules, contributing to chronic inflammation, or "inflammaging," linked to age-related diseases. Scientists at Sanford Burnham Prebys discovered that mitochondria control a DNA repair protein's ability to suppress this inflammation. The study, published in *Nature Communications*, showed that the tumor protein p53 suppressed SASP [senescence-associated secretory phenotype] and the formation of cytoplasmic chromatin fragments (CCF) [bits of damaged DNA in the cytoplasm], which trigger the immune system. Senescent cells also experience mitochondrial dysfunction, leading to CCF formation and reduced p53 expression. Researchers identified a cellular circuit that promotes DNA repair while suppressing inflammation in senescent cells. Existing drugs can modify this pathway in cultured cells and mice, suggesting potential treatments for healthier aging.