Inhibition of IL-11 signalling extends mammalian healthspan and lifespan
Researchers found inhibiting IL-11 signaling extends mammal healthspan and lifespan. Deleting Il11 or Il11ra1 in mice protects against aging-related issues. Anti-IL-11 treatment improves metabolism, muscle function, and extends mouse lifespan significantly.
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Researchers have discovered that inhibiting IL-11 signaling can extend the healthspan and lifespan of mammals. IL-11, a pro-inflammatory cytokine, is upregulated with age and plays a role in regulating pathways related to aging and disease. Deleting Il11 or Il11ra1 in mice protected against metabolic decline, multi-morbidity, and frailty in old age. Administering anti-IL-11 to older mice improved metabolism, muscle function, and reduced aging biomarkers. Genetic deletion of Il11 extended the lives of mice by nearly 25%, while treatment with anti-IL-11 increased median lifespan by around 22.5% to 25% in male and female mice. The study suggests that inhibiting IL-11, currently being tested in clinical trials for lung disease, could be a potential strategy to address aging-related issues in older individuals. The research highlights the importance of understanding the impact of interventions on both healthspan and lifespan, with a focus on the role of inflammation in aging processes.
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