Core Concepts
Inhibition of the pro-inflammatory cytokine IL-11 can extend healthspan and lifespan in mice.
Abstract
The article examines the role of the pro-inflammatory cytokine IL-11 in the aging process and its impact on healthspan and lifespan in mammals. As mice age, IL-11 levels increase across cell types and tissues, regulating an ERK-AMPK-mTORC1 axis that contributes to cellular, tissue, and organismal-level aging pathologies.
The key findings are:
Deletion of Il11 or Il11ra1 (the IL-11 receptor) protects against metabolic decline, multi-morbidity, and frailty in old age.
Administration of anti-IL-11 antibodies to 75-week-old mice for 25 weeks improves metabolism, muscle function, and reduces aging biomarkers and frailty in both sexes.
Genetic deletion of Il11 extends the lifespan of mice by 24.9% on average.
Treatment with anti-IL-11 antibodies from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and female mice by 25%.
The authors suggest that anti-IL-11 therapy, currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to target aging pathologies in older people.
Stats
Genetic deletion of Il11 extended the lifespan of mice by 24.9% on average.
Treatment with anti-IL-11 antibodies from 75 weeks of age until death extended the median lifespan of male mice by 22.5% and female mice by 25%.
Quotes
"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."
"Together, these results demonstrate a role for the pro-inflammatory factor IL-11 in mammalian healthspan and lifespan."