CCND1 gene linked to chronic inflammation in senescent cells

Researchers at the Sanford Burnham Prebys Medical Discovery Institute and an international team have identified a biological paradox involving the CCND1 gene, which produces the protein cyclin D1. While this gene is traditionally known in oncology for driving cancer by pushing cells to replicate, it also plays a significant role in senescent cells—non-proliferating, “zombie-like” cells that are meant to prevent cancer by halting the cell cycle.

Findings published in Nature Aging reveal that in these non-dividing senescent cells, cyclin D1 acts as a driver of chronic inflammation. As people age, immune cells become less effective at removing these senescent cells, leading to their accumulation and the subsequent release of inflammatory molecules. This discovery suggests that targeting the CCND1 gene could provide a pathway for future therapies aimed at reducing sustained inflammation and promoting healthier aging.