In the lightless depths of the Arctic, a creature that outlives civilizations has quietly preserved something humanity is losing by the millions: the ability to see. Greenland sharks, alive for up to four centuries, carry retinas that remain structurally pristine long past the age when human eyes begin to fail — and the molecular machinery responsible may now offer a path toward treating the degenerative vision conditions that darken the lives of over 200 million people. Scientists studying these ancient animals remind us that the most consequential medical discoveries often begin not with a c
Greenland shark's ageless eyes reveal anti-aging secrets for human vision
The structure of the eye looks beautiful. It's basically pristine.
Why does a shark living in complete darkness need eyes that work so well?
That's the puzzle at the heart of this. The shark probably isn't using vision much at 3,000 meters down, but it may use its eyes to navigate shallower waters or to detect the faint bioluminescence of prey. The point is, whatever it's doing with those eyes, they're not falling apart the way ours do.
The parasites attached to the eyes—don't those just blind the shark?
They reduce clarity, yes. But the retina underneath stays intact. The shark can still detect light and movement. It's like looking through frosted glass instead of clear glass. You lose detail but you're not in darkness.
So the real discovery is about these DNA repair genes?
Exactly. The shark has ERCC1 and ERCC4 running at high levels, constantly fixing damage before it becomes permanent. We have those genes too, but we don't use them the same way. Understanding why the shark does this—and how—could let us do the same thing in human eyes.
Is this close to becoming a treatment?
Not yet. This is basic science. The researchers are saying: here's a mechanism that works. Now we need to figure out how to activate it in humans. That could mean gene therapy, or drugs that boost these repair pathways. But it's early.
How many people could this actually help?
Over 200 million people globally have some form of age-related vision loss. Many of them lose sight because their rod cells—the same cells the shark protects so well—gradually fail. If we could slow or stop that process, the impact would be enormous.
What's the chance this actually works in humans?
Unknown. But the fact that the same genes exist in us, and that they're clearly doing something powerful in the shark, makes it worth pursuing. Nature has already solved this problem once. We're just trying to learn the solution.
Il Polso
- Over 200 million people worldwide are losing their sight to conditions like macular degeneration and retinitis pigmentosa, diseases for which medicine has long lacked a meaningful answer.
- Greenland sharks — scarred, slow, and parasitized — nonetheless maintain near-perfect retinal tissue past their first century of life, a biological contradiction that demanded explanation.
- Researchers found the answer in two DNA repair genes, ERCC1 and ERCC4, expressed at unusually high levels in shark retinas, acting as a relentless molecular maintenance crew against cellular decay.
- Humans carry these same genes but deploy them far less aggressively, and when they fail in people, the result is accelerated aging and vision loss — suggesting the gap between us and the shark is one of degree, not kind.
- Scientists are now designing genetic and molecular therapies to amplify these repair pathways in human eyes, translating four hundred years of shark evolution into potential clinical medicine.
In the lightless depths of the Arctic, a creature that outlives civilizations has quietly preserved something humanity is losing by the millions: the ability to see. Greenland sharks, alive for up to four centuries, carry retinas that remain structurally pristine long past the age when human eyes begin to fail — and the molecular machinery responsible may now offer a path toward treating the degenerative vision conditions that darken the lives of over 200 million people. Scientists studying these ancient animals remind us that the most consequential medical discoveries often begin not with a cure in mind, but with a simple, open question about how life endures.
The Greenland shark appears, at first glance, to be a portrait of deterioration — slow-moving, scarred, its corneas often colonized by parasitic crustaceans. Yet this animal, which can survive for roughly 400 years in the frigid North Atlantic and Arctic, conceals something extraordinary: its eyes barely age at all.
When researchers examined the retinas of ten Greenland sharks between 100 and 134 years old, they found tissue that was, in the words of senior author Dorota Skowronska-Krawczyk, "basically pristine." The contrast with human eyes is stark. Our rod cells — responsible for vision in low light — accumulate damage over decades, and in millions of people, that process accelerates into blindness.
The sharks' visual system is simpler than ours: they possess only rod cells, no cones, perceiving a colorless world suited to depths of three kilometers. But that simplified system endures. The parasites clouding their corneas reduce image clarity, yet the retina and its neural pathways remain intact and light-responsive across centuries.
The key lies in two DNA repair genes — ERCC1 and ERCC4 — expressed at unusually high levels in shark retinal tissue. These genes function as a constant molecular repair crew, correcting DNA damage before it becomes permanent. Humans carry the same genes but activate them far less powerfully. When they malfunction in people, premature aging and vision loss follow.
For the more than 200 million people living with age-related vision conditions, this opens a genuine possibility. Visual neuroscientist Patricia Jusuf noted that rod cells are typically the first to fail in human degenerative diseases, and that boosting DNA repair pathways could slow or halt that loss. Genetic and molecular therapies targeting these mechanisms are now being planned.
The researchers are careful to note that this discovery was not engineered — it emerged from curiosity about how an animal could live so long. Skowronska-Krawczyk emphasized that basic science, driven by questions rather than predetermined outcomes, made it possible. Closer to home, two relatives of the Greenland shark inhabit waters near Australia and New Zealand, their biology largely unstudied. They may carry their own secrets, waiting for someone willing to look.
The Greenland shark is a creature that seems built for decline. It moves through the ocean at a crawl, its skin mottled and scarred, its eyes clouded and often infested with parasitic crustaceans that hook into the cornea like tiny white tassels. Yet this animal, which can live for roughly 400 years in the frigid waters of the North Atlantic and Arctic, harbors a secret that scientists are only now beginning to understand: its eyes barely age at all.
Researchers examining the eyes of ten dead Greenland sharks, each between 100 and 134 years old, found something remarkable. The retinal tissue—the light-sensing layer at the back of the eye—showed almost no signs of deterioration. "The structure of the eye looks beautiful," said Dorota Skowronska-Krawczyk, a senior author of the study published in Nature Communications. "It's basically pristine." This finding matters because human eyes, by contrast, accumulate damage over decades. The rod cells that allow us to see in dim light gradually fail. In millions of people worldwide, this process accelerates into blindness.
To understand how the shark maintains such youthful eyes across centuries, the research team looked closely at the organ's cellular machinery. Greenland sharks, unlike humans, possess only rod cells—the light receptors designed for darkness. They lack cone cells entirely, meaning they see their world in shades of gray, without color or fine detail. This adaptation makes sense for an animal that spends most of its life in pitch-black waters three kilometers deep. Yet even with this simplified visual system, the sharks' eyes remain functional. The parasites that colonize their corneas reduce image clarity, but the underlying retina and its neural pathways stay intact and responsive to light.
The breakthrough lies in the genes. The researchers identified unusually high expression of two DNA repair genes—ERCC1 and ERCC4—in the shark's retinal tissue. These genes are the cellular equivalent of a repair crew, constantly fixing damage to DNA before it accumulates into permanent harm. Humans possess these same genes, but we do not activate them with the same vigor. When these genes malfunction in people, the results are severe: premature aging and accelerated vision loss. The implication is striking: the shark has solved a problem that has plagued human medicine for decades.
For the more than 200 million people worldwide living with age-related vision loss—conditions like macular degeneration and retinitis pigmentosa—this discovery opens a door. Patricia Jusuf, a visual neuroscientist at the University of Melbourne, noted that rod cells are often the first casualties in these human diseases. "Being able to manipulate DNA repair pathways to slow down or halt degeneration of these rod photoreceptors in humans holds great benefits," she said. The path forward involves genetic and molecular therapies designed to boost the same repair mechanisms the shark has perfected over evolutionary time.
Yet the researchers emphasize that this knowledge emerged not from hunting for a cure, but from simple curiosity about how an animal could live so long. Skowronska-Krawczyk stressed the importance of funding basic science—research driven by questions rather than predetermined outcomes. "It's only through the curiosity of researchers that the long life-span of the Greenland shark was discovered," she said. "And only then could we start working and thinking about applications."
The work also hints at untapped potential closer to home. Two relatives of the Greenland shark—the southern sleeper shark and the Pacific sleeper shark—inhabit waters around Australia and New Zealand. Little is known about their biology or their eyes. They may carry their own genetic secrets, waiting for researchers willing to look.
Citazioni salienti
If we can study that and work out what that mechanism is, they could have biomedical applications.— Lily Fogg, marine biologist and lead study author, University of Basel
Being able to manipulate DNA repair pathways to slow down or halt degeneration of these rod photoreceptors in humans holds great benefits for the more than 200 million people affected by visual loss.— Patricia Jusuf, visual neuroscientist, University of Melbourne