In a groundbreaking study, scientists have found that turning off a specific protein, interleukin 11 (IL-11), can dramatically increase the healthy lifespan of mice.
Researchers from the UK’s Medical Research Council Laboratory and Imperial College London, in collaboration with Duke-NUS Medical School in Singapore, conducted experiments that revealed the profound impact of deactivating this protein.
By deleting the gene responsible for IL-11 in mice, the researchers were able to extend the animals’ lifespans by over 20% on average, a discovery that could pave the way for future anti-aging treatments in humans.
Extending Lifespan Through Protein Deactivation
To test their hypothesis, the scientists treated 75-week-old mice—roughly the equivalent of a 55-year-old human—with an anti-IL-11 antibody. This drug effectively blocks the action of the IL-11 protein within the body.
The results were astonishing. Mice that received the treatment lived significantly longer, with males seeing an average lifespan extension of 22.4% and females an even more impressive 25%. The treated mice lived an average of 155 weeks, far exceeding the 120-week lifespan of untreated mice.
The effects of the treatment were not limited to increased longevity; it also reduced deaths from cancer and mitigated the onset of diseases commonly associated with aging, such as fibrosis, chronic inflammation, and metabolic disorders. These are considered the hallmarks of aging. Importantly, the researchers noted that there were very few side effects observed in the treated animals, making this intervention not only effective but also safe.
“These findings are very exciting,” said Professor Stuart Cook, one of the study’s co-authors, published in the journal Nature.
“The treated mice had fewer cancers, and were free from the usual signs of aging and frailty, and we also saw reduced muscle wasting and improvement in muscle strength.”
Potential Implications for Human Aging
Although the study was conducted on mice, the results suggest that IL-11 may play a similar role in human aging.
“While these findings are only in mice, it raises the tantalizing possibility that the drugs could have a similar effect in elderly humans. Anti-IL-11 treatments are currently in human clinical trials for other conditions, potentially providing exciting opportunities to study its effects in aging humans in the future,” added Cook.
This discovery offers hope that anti-IL-11 treatments could one day be used to slow the aging process in humans. By preventing diseases that lead to frailty, muscle loss, and other aging symptoms, it could provide a means of not just living longer, but living healthier lives well into old age.
The Role of IL-11 in Aging and Disease
Researchers have been investigating IL-11 for years, and in 2018, they discovered that it is a pro-fibrotic and pro-inflammatory protein. This revelation overturned decades of previous belief that IL-11 had anti-fibrotic and anti-inflammatory properties. The team’s research into this protein has now shown that it plays a critical role in the aging process.
Assistant Professor Anissa Widjaja, a co-author of the study, recalled how their investigation into IL-11 beganback in 2017.
“A collaborator of ours sent us some tissue samples for another project. Out of curiosity, I ran some experiments to check for IL-11 levels. From the readings, we could clearly see that the levels of IL-11 increased with age and that’s when we got really excited!” Widjaja explained.
The rising levels of IL-11, they discovered, contribute to various negative effects in the body, including inflammation and impaired healing and regeneration of organs after injury.
“Although our work was done in mice, we hope that these findings will be highly relevant to human health, given that we have seen similar effects in studies of human cells and tissues,” she added.
IL-11 and the Human Aging Process
Interestingly, scientists have speculated that IL-11 may be an evolutionary leftover in humans. While this protein is crucial for limb regeneration in certain animal species, it is thought to be mostly redundant in humans.
However, the research indicates that after the age of 55, IL-11 production increases in humans, potentially leading to chronic inflammation, fibrosis in organs, and muscle wasting. These conditions contribute to aging symptoms such as sarcopenia, frailty, and cardiac fibrosis.
When individuals experience two or more of these aging-related conditions simultaneously, it is referred to as multi-morbidity. Multi-morbidity encompasses a wide range of chronic conditions, including cardiovascular disease, diabetes, lung disease, and the decline of vision and hearing. These issues severely impact quality of life in old age and are currently treated individually rather than as part of a larger aging process.
As Professor Cook noted, “The IL-11 gene activity increases in all tissues in the mouse with age, causing loss of function across the whole body, ranging from eyesight to hearing, from muscle to hair, and from the pump function of the heart to the kidneys.”
This widespread effect of IL-11 highlights the importance of understanding and potentially targeting this protein in future treatments for aging.
Future of Anti-IL-11 Treatments
The current study offers a promising avenue for treating age-related diseases through anti-IL-11 therapies. Human clinical trials are already underway to test the efficacy of these treatments for other medical conditions, and if successful, they may open up opportunities to use the same drugs to slow down aging in humans.
However, more research is needed to determine whether these findings in mice will translate effectively to human health.
Ultimately, the success of these treatments in human clinical trials will dictate whether doctors consider using anti-IL-11 drugs as a method to combat aging and multi-morbidity.
The research was primarily funded by the National Medical Research Council in Singapore and the UK’s Medical Research Council, with significant implications for the future of aging research and potential breakthroughs in human longevity.
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