- Scientists have discovered that deactivating a protein called IL-11 can extend the healthy lifespan of mice by nearly 25%, raising the potential for similar benefits in humans.
- Researchers found that removing the IL-11 gene or using an anti-IL-11 antibody dramatically increased the lifespan and health of aging mice.
- These findings suggest that anti-IL-11 treatments could combat age-related diseases with minimal side effects, offering a promising avenue for future human trials.
The results were significant: mice treated with the anti-IL-11 drug from 75 weeks of age until their death showed a median lifespan extension of 22.5% in males and 25% in females, living an average of 155 weeks compared to 120 weeks in untreated mice.
In addition, the treatment significantly decreased cancer-related deaths in the animals and also reduced various diseases associated with fibrosis, chronic inflammation, and poor metabolism, which are typical of aging.
Importantly, only minimal side effects were observed.
Previously, scientists have suggested that IL-11 is an evolutionary hangover in humans.
While essential for limb regeneration in some animals, it is largely considered redundant in humans.
However, after the age of 55, IL-11 production increases in humans and has been linked to chronic inflammation, fibrosis in organs, metabolic disorders, muscle wasting (sarcopenia), frailty, and cardiac fibrosis — many signs of aging.
When an individual experiences two or more of these conditions, it is termed multimorbidity, encompassing a variety of ailments such as lung disease, cardiovascular disease, diabetes, and sensory decline, among others.
IL-11 gene activity increases in all mouse tissues with age, and when activated, it leads to multimorbidity, manifesting as age-related diseases and functional decline throughout the body, affecting vision, hearing, muscle strength, hair, heart function, and kidneys.
