People could live up to 25 per cent longer in better health if a redundant gene is switch off, according to Imperial College London. Kath Hudson reports
Imperial College research has exciting implications for ageing / photo: Shutterstock/PeopleImages.com - Yuri A
Research from Imperial College London indicates that switching off a protein could lead to people living up to 25 per cent longer and enjoying better health in their later years.
Back in 2017, Imperial College discovered that the protein interleukin 11 (IL-11) plays a key role in the scarring process which causes heart, kidney and liver failure, so inhibiting the gene can prevent fibrosis – the build-up of excessive connective tissue in organs – which contributes to organ failure.
Further research has shown that switching off the gene could have more far-reaching health benefits and the potential to delay many of the issues that come with ageing, including the loss of vision, hearing, hair and muscle, as well as improving lung function and metabolism, reducing the incidences of cancer and significantly adding to healthy lifespan.
Increasing healthspan and lifespan This research is also exciting because so far the indications are showing that inhibiting this gene could extend healthspan as well as lifespan.
Professor Stuart Cook, from the Medical Research Council Laboratory of Medical Science, Imperial College – who led the research – says: “These findings are very exciting. Previously proposed life-extending drugs and treatments have either had poor side-effect profiles, or don’t work in both sexes, or could extend life, but not healthy life. However this does not appear to be the case for IL-11.”
Interleukins are proteins involved in relaying signals between the cells and help regulate cell growth, differentiation and movement. They’re important for immune responses, inflammation and fibrosis. However, IL-11, is believed to be an evolutionary hangover for humans: while it’s vital for limb regeneration in some animal species, it’s thought to be largely redundant in humans.
More interleukin 11 means faster ageing After the age of 55, increasing levels of IL-11 are produced and previous research has linked this to chronic inflammation, fibrosis in organs, metabolism disorders, muscle wasting, frailty and cardiac fibrosis.
Clinical trials of anti IL-11 therapy are currently in the early stages for treating fibrotic lung disease and may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people. Early trial data suggests the intervention is safe.
In the future there is the possibility of a therapeutic drug being given in later life, or – more controversially – gene editing at birth.
The research was published in Nature and partly funded by the Medical Research Council.
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People could live up to 25 per cent longer in better health if a redundant gene is switch off, according to Imperial College London. Kath Hudson reports
Imperial College research has exciting implications for ageing / photo: Shutterstock/PeopleImages.com - Yuri A
Research from Imperial College London indicates that switching off a protein could lead to people living up to 25 per cent longer and enjoying better health in their later years.
Back in 2017, Imperial College discovered that the protein interleukin 11 (IL-11) plays a key role in the scarring process which causes heart, kidney and liver failure, so inhibiting the gene can prevent fibrosis – the build-up of excessive connective tissue in organs – which contributes to organ failure.
Further research has shown that switching off the gene could have more far-reaching health benefits and the potential to delay many of the issues that come with ageing, including the loss of vision, hearing, hair and muscle, as well as improving lung function and metabolism, reducing the incidences of cancer and significantly adding to healthy lifespan.
Increasing healthspan and lifespan This research is also exciting because so far the indications are showing that inhibiting this gene could extend healthspan as well as lifespan.
Professor Stuart Cook, from the Medical Research Council Laboratory of Medical Science, Imperial College – who led the research – says: “These findings are very exciting. Previously proposed life-extending drugs and treatments have either had poor side-effect profiles, or don’t work in both sexes, or could extend life, but not healthy life. However this does not appear to be the case for IL-11.”
Interleukins are proteins involved in relaying signals between the cells and help regulate cell growth, differentiation and movement. They’re important for immune responses, inflammation and fibrosis. However, IL-11, is believed to be an evolutionary hangover for humans: while it’s vital for limb regeneration in some animal species, it’s thought to be largely redundant in humans.
More interleukin 11 means faster ageing After the age of 55, increasing levels of IL-11 are produced and previous research has linked this to chronic inflammation, fibrosis in organs, metabolism disorders, muscle wasting, frailty and cardiac fibrosis.
Clinical trials of anti IL-11 therapy are currently in the early stages for treating fibrotic lung disease and may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people. Early trial data suggests the intervention is safe.
In the future there is the possibility of a therapeutic drug being given in later life, or – more controversially – gene editing at birth.
The research was published in Nature and partly funded by the Medical Research Council.
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disparate information from multiple systems to be aggregated into one dataset, to support
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