Preprint: genetic deletion of STING extends median lifespan and reduces liver ageing in mice

A preprint posted to bioRxiv by researchers at Cold Spring Harbor Laboratory reports that genetic deletion of STING — the stimulator of interferon genes, a central component of the cGAS-STING innate immune signalling pathway — extends median lifespan in mice and markedly reduces the accumulation of age-related liver pathology.

The cGAS-STING pathway is activated by cytosolic DNA, a signal associated with cellular damage, viral infection, and the release of mitochondrial or nuclear DNA fragments that accumulate with ageing. Chronic, low-grade activation of this pathway has been proposed as a contributor to the sterile inflammation, commonly termed inflammageing, that accompanies mammalian ageing. The new preprint provides whole-lifespan data in STING-knockout mice, complementing earlier work showing that acute STING inhibition can reduce neuroinflammation and tissue damage in shorter experimental windows.

The authors report that STING-deficient animals showed significantly improved survival curves compared with wild-type controls, alongside histological evidence of reduced hepatic steatosis and fibrosis at late ages. They propose that STING represents a promising target for interventions aimed at extending healthy lifespan, though they note that the global, lifelong deletion model used in this study does not directly translate to pharmacological inhibition strategies in adult animals, which would involve different temporal and tissue-specific dynamics.

As a preprint, this work has not yet been peer-reviewed. Independent replication and peer scrutiny will be necessary before the findings can be interpreted with confidence. The research is relevant to the biology of ageing and to researchers working on innate immunity and longevity, but does not carry immediate translational implications.