Hormonal
Inhibition of IL-11 signaling through genetic deletion or therapeutic antibody administration extends mammalian healthspan and lifespan by mitigating age-associated metabolic decline, frailty, and tissue fibrosis.
This research suggests that targeting the IL-11 pathway could be a viable strategy for extending healthspan and lifespan in humans. While the study was conducted in mice, the findings support the potential of anti-IL-11 therapies, which are already in clinical trials for other conditions, to mitigate age-related decline. For now, this remains a preclinical finding, but it highlights IL-11 as a promising target for future longevity interventions.
Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age. Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes. In lifespan studies, genetic deletion of Il11 extended the lives of mice of both sexes, by 24.9% on average. Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%.
Why this rating
The study utilizes rigorous genetic models (knockouts) and pharmacological interventions (antibodies) in mice with robust statistical analysis, demonstrating consistent effects across sexes and multiple tissues.
Source
Inhibition of IL-11 signalling extends mammalian healthspan and lifespan
Anissa A. Widjaja et al. · Nature · 2024
DOI 10.1038/s41586-024-07701-9
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