Blocking this protein boosts lifespan by 25%, study finds
By “switching off” a protein called IL-11, they significantly increased the healthy lifespan of mice by nearly 25%.
‘Switching off’ a protein called IL-11 can significantly increase the healthy lifespan of mice by almost 25%. (CREDIT: Creative Commons)
Researchers at the Medical Research Council Laboratory of Medical Science and Imperial College London have made a breakthrough discovery. By "switching off" a protein called IL-11, they significantly increased the healthy lifespan of mice by nearly 25%.
Collaborating with Duke-NUS Medical School in Singapore, the team deleted the gene responsible for producing IL-11 (interleukin 11) in mice. This genetic modification extended the mice's lives by over 20% on average. In addition, they treated 75-week-old mice, roughly equivalent to 55-year-old humans, with an anti-IL-11 antibody drug that inhibits IL-11 in the body.
The results, published in Nature, were striking. Mice treated with the anti-IL-11 drug from 75 weeks of age until death had their median lifespan extended by 22.4% in males and 25% in females. These treated mice lived an average of 155 weeks compared to the 120 weeks of untreated mice.
The treatment notably reduced cancer-related deaths and decreased diseases caused by fibrosis, chronic inflammation, and poor metabolism—common markers of aging. Few side effects were observed.
“These findings are very exciting,” said Professor Stuart Cook, co-corresponding author from the Medical Research Council Laboratory of Medical Science (MRC LMS), Imperial College London, and Duke-NUS Medical School. “The treated mice had fewer cancers and were free from the usual signs of aging and frailty. We also saw reduced muscle wasting and improvement in muscle strength. In other words, the old mice receiving anti-IL11 were healthier.”
Professor Cook emphasized the uniqueness of this treatment, noting that previously proposed life-extending drugs either had poor side-effect profiles, didn't work in both sexes, or extended lifespan without improving healthy life. “This does not appear to be the case for IL-11,” he added.
While the current findings are in mice, they suggest the tantalizing possibility that similar effects could be seen in elderly humans. Anti-IL-11 treatments are currently in human clinical trials for other conditions, which may offer exciting opportunities to study its effects on aging in humans.
The team has been studying IL-11 for many years. In 2018, they were the first to demonstrate that IL-11 is a pro-fibrotic and pro-inflammatory protein, contradicting years of incorrect characterization as anti-fibrotic and anti-inflammatory.
Assistant Professor Anissa Widjaja, also a co-corresponding author from Duke-NUS Medical School, shared the origins of the project. “This project started back in 2017 when a collaborator sent us tissue samples for another project. Out of curiosity, I checked for IL-11 levels. We saw that IL-11 levels increased with age, and that’s when we got really excited!”
“We found these rising levels contribute to negative effects in the body, such as inflammation and preventing organs from healing and regenerating after injury. Although our work was done in mice, we hope that these findings will be highly relevant to human health, given similar effects observed in human cells and tissues.”
The research marks a significant step toward understanding aging better. “We have demonstrated, in mice, a therapy that could potentially extend healthy aging by reducing frailty and the physiological manifestations of aging,” said Widjaja.
Previous studies suggested that IL-11 is an evolutionary remnant in humans. While it is vital for limb regeneration in some animals, it is largely redundant in humans. However, after about age 55, humans produce more IL-11, which is linked to chronic inflammation, fibrosis in organs, metabolism disorders, muscle wasting (sarcopenia), frailty, and cardiac fibrosis—all signs of aging.
When multiple such conditions occur in an individual, it is known as multimorbidity, which includes lung disease, cardiovascular disease, diabetes, vision and hearing decline, and more. Professor Cook explained, “IL-11 gene activity increases in all tissues in the mouse with age. When it gets turned on, it causes multimorbidity, which is diseases of aging and 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.”
Multimorbidity and frailty are major global healthcare challenges, recognized by leading health bodies, including the NHS and WHO. Currently, there is no treatment for multimorbidity other than addressing each underlying cause separately.
The researchers caution that while these results in mice are promising, the safety and effectiveness of these treatments in humans need further validation through clinical trials. The study was funded by the National Medical Research Council (Singapore) and the Medical Research Council (UK).
Note: Materials provided above by the The Brighter Side of News. Content may be edited for style and length.
Like these kind of feel good stories? Get the Brighter Side of News' newsletter.
