Humans have long dreamed about finding the fountain of youth - a supposedly fictional source that could offer us eternal life (or honestly just knock a few years off and we’d still be happy).
But now scientists have discovered a protein in mammals that actually increases their expected lifespan when it is present in higher quantities.
And conversely, cause animals to die earlier when it is taken away.
The study, from Cape Western Reserve University identified a new molecular pathway, controlled by a proteins called KLF, that is essential to bodily function because it controls a process called autophagy.
Autophagy is a natural recycling process in the body that clears away useless debris such as misfolded proteins or molecular byproducts that naturally build up over time.
Loss of control over this mechanism is a classic hallmark of getting older, allowing toxic proteins to aggregate.
This build-up creates obstacles to our cells surviving in the form of age-associated disorders such as hypertension, heart disease, and dementia.
Nelson Hsieh, first author, said: “As our population ages, we need to understand what happens to our heart and arteries, as we rely on them to function perfectly later and later on in our lives.”
The team speculated that having a greater presence of this KLF protein, could directly help and tested their theory by artificially giving a sample of worms (Caenorhabditis elegans) an excess of the protein.
And found that they did indeed live longer than other normal worms.
Hsieh said: “We can actually get these small worms to live for longer or shorter time periods.”
Not only that, but the study published in Nature Communications, also looked at a group of mice with excess levels of these proteins, and demonstrated a delay in blood vessel dysfunction associated with ageing.
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“Since this same family of proteins also exists in mammals, what is really exciting is that our data suggests the KLFs also have similar effects on aging in mammals too,” said Hsieh.
The next step will be to study the precise mechanisms underlying how autophagy in cells lining blood vessels contributes to improved blood vessel function and seek strategies to target KLF in humans.
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