Published on: Jan 05, 2026
Advanced age is commonly accompanied by chronic tissue inflammation, a key contributor to many age-related diseases, including cardiovascular disease and cancer.
One major source of this inflammatory state is the accumulation of senescent cells—cells that cease dividing but persist in aging tissues. Senescent cells are characterized by two hallmark features: enlargement of the nucleolus and the release of pro-inflammatory factors collectively known as the senescence-associated secretory phenotype (SASP).
While the SASP is known to drive chronic inflammation and disease, the biological significance of nucleolar enlargement during aging has remained poorly understood.
In a study led by researchers at the Institute of Genetics and Cancer, investigators identified the nucleolar protein TIF-IA as a key regulator linking nucleolar expansion to inflammatory signaling in senescent cells. The team found that TIF-IA accumulates in senescent cells and in intestinal tissue across multiple mouse models of aging.
This accumulation was traced to DNA damage—a hallmark of cellular senescence and aging tissues. Under normal conditions, TIF-IA levels are regulated by the protein p62, which targets it for degradation. However, DNA damage disrupts the interaction between p62 and TIF-IA, allowing TIF-IA to build up within the cell.
By experimentally reducing TIF-IA levels, the researchers demonstrated that this protein is essential for both nucleolar enlargement and activation of the SASP. Conversely, artificially increasing TIF-IA was sufficient to induce nucleolar expansion, trigger SASP factor secretion, and promote cellular senescence.
Together, these findings reveal a previously unrecognized pathway connecting DNA damage, nucleolar remodeling, and inflammatory signaling in aging tissues, offering new insight into the mechanisms underlying age-related inflammation and disease.
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