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Mouse Study: Inhibiting IL-11 Slows Aging and Extends Lifespan

A new study published in the journal Nature found that inhibiting the protein IL-11 extended the lifespan of mice by about 25% and reduced age-related diseases and markers of aging. This is a finding in mice only, and a similar effect in humans has not yet been proven. The researchers conducted experiments on mice and discovered that turning off IL-11 improved metabolism and muscle function and reduced the incidence of cancer.

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Scientists, including researchers from Imperial College London and other countries, report a finding that may slow the aging process and reduce age-related diseases.
A new study published in the scientific journal Nature found that inhibiting the protein IL-11 extended the lifespan of mice by about 25%. It is important to emphasize: this is in mice only, and a similar effect in humans has not yet been proven.

Study Findings

The researchers conducted experiments on mice and discovered that turning off the protein interleukin-11 (IL-11) reduced the incidence of cancer in mice,
improved metabolism and muscle function, and reduced markers of aging and frailty.
The study also observed additional improvements in the health of the mice as they aged.
Mice treated with the antibody lived on average significantly longer than untreated mice.

Effects on Health and Longevity

The study showed that turning off IL-11 in mice improved muscle function, increased metabolism, and reduced levels of aging and frailty markers.
The mice treated with IL-11 antibodies showed less cancer and were free from typical signs of aging and frailty.

Human Potential of the Drug

Although the study was conducted only on mice, the scientists hope that inhibiting IL-11 may yield similar results in older people, which still needs to be proven in clinical trials.
IL-11 is a pro-inflammatory protein whose levels increase with age, and it is linked to scarring, tissue thickening, and inflammation processes that contribute to disease and aging.
An antibody against IL-11 is already in early stages of clinical trials for fibrotic lung disease, which may open the door to testing its effect on aging in the future.

Mechanism of Action of IL-11

In the study, IL-11 was found to be a pro-inflammatory protein from the IL-6 cytokine family, activating the ERK, AMPK, and mTORC1 signaling pathways.
In older mice, IL-11 expression is elevated in various cells and tissues, and turning off the protein protected the mice from metabolic decline, frailty, and increased disease as they aged.

Study Results in Mice

The study found that administering IL-11 antibodies to mice aged 75 weeks and older improved muscle function, increased metabolism, and lowered levels of aging and frailty markers.
Turning off the IL-11 gene extended the lifespan of the mice by about 24.9%, and treatment of 75-week-old mice with IL-11 antibodies extended the lifespan of males by 22.5% and females by 25%.

Effects on Human Cells

IL-11 is linked to senescence in human cells and accelerates aging processes and worsens metabolic functions.
Cells treated with IL-11 antibodies showed improved metabolism, reduced aging characteristics, and decreased inflammation.

Conclusions

The study's findings highlight the negative role of the pro-inflammatory cytokine IL-11 in the lifespan and health of mammals.
The study found that IL-11 antibodies improved metabolic parameters and muscle function and reduced the incidence of cancer in mouse models.
These findings suggest that pharmacological modulation of IL-11 may be of value in treating cancer and fibrotic lung diseases.

References: https://www.nature.com/articles/s41586-024-07701-9

Sources and citations

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