Highlights

  • Scientists discovered that deactivating the IL-11 protein extends the healthy lifespan of mice by up to 25%.
  • IL-11 deletion and anti-IL-11 antibodies significantly reduced age-related diseases, particularly cancer.
  • The research, published in Nature, suggests potential applications in human aging and multimorbidity treatments.

 

IMAGE SHOWING THE KNOCKOUT MICE THAT DO NOT PRODUCE IL-11 ON THE LEFT, AND NORMALLY AGEING MICE ON THE RIGHT, AT 90-95 WEEKS OLD.

Inhibiting IL-11 can extend the lifespan

Researchers from the Medical Research Council Laboratory of Medical Science, Imperial College London, and Duke-NUS Medical School have found that inhibiting the protein IL-11 can extend the lifespan and health span of mice. By deleting the gene for IL-11 or administering an anti-IL-11 antibody to older mice, their median lifespan increased by 22.4% in males and 25% in females. These treatments reduced cancer and diseases linked to fibrosis, chronic inflammation, and poor metabolism, with few side effects. The results, published in Nature, highlight IL-11 as a pro-fibrotic and pro-inflammatory protein that contributes to ageing. This discovery opens possibilities for similar effects in humans, as anti-IL-11 treatments are already in clinical trials for other conditions. The research underscores IL-11’s role in promoting multimorbidity and frailty, offering a promising direction for future therapies aimed at improving healthy ageing.

Reference

10.1038/s41586-024-07701-9