Researchers have discovered a potential breakthrough in extending mammalian healthspan and lifespan through the inhibition of IL-11 signaling. IL-11, a pro-inflammatory cytokine of the IL-6 family, has been found to have a negative impact on age-associated diseases and lifespan. As mice age, IL-11 levels increase, affecting critical pathways such as ERK, AMPK, and mTORC1, which are essential for healthspan and lifespan.
Studies have shown that deletion of Il11 or Il11ra1 in mice can protect against metabolic decline, multi-morbidity, and frailty in old age. Administering anti-IL-11 to 75-week-old mice for 25 weeks has been shown to improve metabolism, muscle function, and reduce aging biomarkers and frailty in both male and female mice. Lifespan studies revealed that genetic deletion of Il11 extended the lives of mice by an average of 24.9%, with treatment of anti-IL-11 from 75 weeks of age until death extending the median lifespan of male mice by 22.5% and female mice by 25%.
These findings highlight the significant role of IL-11 in mammalian healthspan and lifespan. The potential for anti-IL-11 therapy, currently being explored in early-stage clinical trials for fibrotic lung disease, presents an exciting opportunity to investigate the effects of IL-11 inhibition on aging pathologies in older individuals.
