Researchers have found that deactivating a protein called IL-11 can significantly boost the healthy lifespan of mice by nearly 25%.
A team of scientists from the Medical Research Council Laboratory of Medical Science and Imperial College London, in collaboration with Duke-NUS Medical School in Singapore, conducted experiments on mice to examine the effects of IL-11. By deleting the gene responsible for producing IL-11, the researchers extended the mice’s lifespan by over 20% on average.
In addition, the researchers administered an anti-IL-11 antibody injection to 75-week-old mice, equivalent to about 55 human years. The results, published in Nature, showed that treating the mice with the anti-IL-11 drug increased the median lifespan by 22.4% in males and 25% in females. The treated mice lived, on average, 155 weeks compared to 120 weeks for untreated mice.
The treatment reduced cancer-related deaths in mice and also mitigated diseases linked to aging, such as fibrosis, chronic inflammation, and metabolic disorders. The researchers noted minimal side effects from the treatment.
Professor Stuart Cook, one of the study’s authors, mentioned that the treated mice displayed improved health, reduced muscle wasting, and enhanced muscle strength, suggesting a reversal of typical signs of aging and frailty.
Previous longevity treatments have often shown poor side effect profiles or lacked effectiveness in both sexes. In contrast, IL-11 treatment demonstrated promising results without significant side effects.
While the study was conducted on mice, the researchers are hopeful that similar effects may be observed in elderly humans. Clinical trials for anti-IL-11 treatments in humans are underway, offering potential opportunities to explore its impacts on aging individuals.
The scientists have been studying IL-11 for several years and in 2018, discovered its pro-fibrotic and pro-inflammatory properties, contrary to prior beliefs that it had anti-fibrotic and anti-inflammatory effects.
Assistant Professor Anissa Widjaja, a co-author of the study, shared that the project began in 2017 when they noticed an increase in IL-11 levels with age. The rise in IL-11 levels was linked to negative effects like inflammation, hindering organ healing, and regeneration after injuries.
The research sheds light on aging processes and presents a potential therapy that could extend healthy aging by addressing frailty and age-related physiological changes.
IL-11 has been considered an evolutionary remnant in humans, contributing to conditions such as chronic inflammation, fibrosis, metabolism disorders, muscle wasting, frailty, and cardiac fibrosis after the age of 55.
Professor Cook emphasized that IL-11 gene activity increases with age in various tissues, leading to multimorbidity, a combination of age-related diseases affecting multiple organs and functions throughout the body.
Multimorbidity and frailty are significant healthcare challenges globally, as they encompass a range of conditions including lung disease, cardiovascular issues, diabetes, vision and hearing loss, among others.
Presently, there is no specific treatment available for multimorbidity besides managing individual underlying causes separately.
While the study showcased promising outcomes in mice, the safety and efficacy of these treatments in humans necessitate further validation through clinical trials before potential use of anti-IL-11 drugs for age-related conditions.
The study received primary funding from the National Medical Research Council (Singapore) and the Medical Research Council (UK).
