GoKawiilYour DNA is under constant assault. Ultraviolet light, environmental toxins, reactive molecules made during run-of-the-mill metabolism and many other disruptors muck with the instructions that keep life humming along. Thankfully, repair crews are at the ready.
This method to reverse cellular ageing is about to be tested in humans
A typical cell can acquire up to a whopping 100,000 lesions each day. “The vast, vast majority are repaired,” says Morten Scheibye-Knudsen, a translational geroscientist at the University of Copenhagen. “We have very, very efficient repair.”
That’s a good thing for a couple of reasons. First, unrepaired or poorly repaired damage can introduce mutations, which can contribute to cancer. And second, DNA damage seems to be one of the main drivers of ageing.
Researchers are amassing evidence that this type of damage underlies many of the hallmarks of ageing, including chronic inflammation, metabolic malfunctions and protein-folding problems1. Such damage triggers cellular alarm bells that can promote inflammation, force cells into an ‘undead’ state known as senescence and even kill them. These responses help the body to grow and thrive, but they become more problematic as we age. The accumulation of beleaguered cells over time is associated with many age-related conditions, including cardiovascular disease, osteoporosis and Alzheimer’s.
That raises a question: if DNA damage is at the root of ageing, can boosting DNA repair slow the process, keeping people healthy for longer? For the first time, this is starting to look like a promising approach, say researchers who study DNA repair2.
Their new optimism comes from studying relatively long-lived species, such as bowhead whales (Balaena mysticetus)3 and naked mole rats (Heterocephalus glaber)4, and looking at the genetics of human centenarians. These studies are pointing to the existence of a great variety of molecular maintenance workers that make for a long and healthy life. A ‘master regulator’ of repair, discovered in 2023, also suggests that these fix-it systems could be enhanced in unison5.
Such findings come alongside a booming interest in longevity more generally, propelled by biotechnology companies, health influencers and governments overseeing ageing populations.
“If you can reduce DNA damage, you would probably have a dramatic effect on the ageing process,” says Paul Robbins, who directs the Nathan Shock Center on Genome Integrity and Aging, which opened last year at the University of Minnesota in Minneapolis. “There are tricks that we can do. But it’s not simple.”
Impressive toolkit
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