We restored it to being a young liver at the most fundamental level
In a laboratory at Bar-Ilan University, Israeli scientists have crossed a threshold long considered theoretical: they did not merely slow the aging of cells, but reversed it. By amplifying the activity of a protein called SIRT6 in already-aged mouse liver tissue, the researchers restored the molecular organization of youth — reordering the genetic filing system that time had scrambled. Published in Nature Communications, the work invites a quiet but profound reconsideration of whether biological aging is a destination or a direction.
- For the first time, scientists have reversed cellular aging in living animals rather than simply slowing its approach — a distinction that redraws the boundary of what medicine might one day attempt.
- The core disruption aging causes is not just wear and tear, but a collapse of order: chromatin, the structure that organizes DNA, destabilizes with age, causing the wrong genes to fire and the right ones to fall silent.
- SIRT6, a protein already linked to longevity, proved capable of more than maintenance — when its activity was boosted in aged mice, their liver cells reorganized back toward youthful molecular patterns.
- The team at Bar-Ilan, led by Haim Cohen alongside researchers Ron Nagar and Zacharia Schwartz, is now confronting the harder question: whether this reversal can travel from mouse livers to human tissues and beyond.
At Bar-Ilan University, Israeli researchers have done something that once seemed to belong to speculation rather than science: they took aged liver cells in mice and restored them to a younger molecular state. The work, published in Nature Communications, centers on a protein called SIRT6 — and what makes it significant is not just what the protein does, but what it was shown to undo.
Earlier research had established that SIRT6 plays a role in healthy aging. Mice with elevated levels of the protein lived longer and maintained better metabolic health. But those experiments only slowed the clock. What Haim Cohen and his team demonstrated is different: they reversed it, taking animals already old at the cellular level and restoring their liver tissue to a younger state.
To grasp the finding, it helps to understand how cells organize themselves. DNA is not free-floating — it is packaged by a structure called chromatin, which functions like a filing system. In young cells, this system is precise: the right genes are active when needed, others remain silent. With age, that order deteriorates. Genes that should work go quiet; genes that should stay silent begin to stir. Cohen described it as a book becoming wrinkled and illegible — the instruction manual of the cell losing its structure.
When the team increased SIRT6 activity in aged mice, the disorganized chromatin in liver cells began to reorganize. Youthful molecular patterns returned. 'We essentially took the liver and rejuvenated it,' Cohen said — restored to clarity at the most fundamental level.
The path from mouse liver cells to human therapies remains long and uncertain. But the underlying principle has now been established: cellular aging may not be irreversible. The question has shifted from whether reversal is possible to how far, and in what tissues, it might one day reach.
In a laboratory at Bar-Ilan University, Israeli researchers have demonstrated something that seemed to belong to the realm of speculation: they took aged liver cells in mice and made them young again. The work, published in Nature Communications, centers on a protein called SIRT6, which appears to have the capacity to undo at least some of the molecular damage that accumulates over time.
The distinction matters. Scientists have long known that SIRT6 plays a role in healthy aging. Earlier studies showed that mice with higher levels of the protein lived longer and maintained better metabolic health. But those experiments worked in one direction only—they slowed the clock. What Haim Cohen and his team, including doctoral researchers Ron Nagar and Zacharia Schwartz, have now shown is different: they reversed it. They took animals that were already old at the cellular level and restored their liver tissue to a younger state.
To understand what happened, it helps to think about how cells organize themselves. Inside every cell sits DNA—the instruction manual for the body. But DNA doesn't float loose. It's packaged and arranged by a structure called chromatin, which acts as a filing system. In young, healthy cells, this system is meticulous. The right genes are accessible and active when they need to be. Others remain switched off. The organization is precise, like a well-kept library where every book is in its place.
With age, that order breaks down. The chromatin becomes unstable. Genes that should be working stop functioning. Genes that should stay silent begin to activate. Cohen described it in simple terms: imagine a book becoming wrinkled and hard to read, its structure no longer organized. That's what happens to the DNA system as an organism ages. The instruction manual becomes illegible.
SIRT6 is a protein that helps regulate DNA repair, gene activity, metabolism, and how cells respond to stress. When Cohen's team increased its activity in aged mice, something unexpected happened. The disorganized chromatin in the liver cells began to reorganize. The genes returned to their proper states. The youthful molecular patterns came back. "We essentially took the liver and rejuvenated it," Cohen said. "We restored it to being a young liver at the most fundamental level—like an instruction book that is clear and properly organised again."
This is the first time SIRT6 has been shown to restore youthful patterns in animals that were already aged, rather than simply slowing the aging process when activated earlier in life. The finding opens a question that researchers and the public will now grapple with: if this works in mouse liver cells, could it work in human cells? Could it work in other tissues? The path from mice to humans is long and uncertain. But the basic principle—that cellular aging may not be a one-way street—has now been demonstrated at the molecular level. The question is no longer whether reversal is possible. It's how far it can go.
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We essentially took the liver and rejuvenated it. We restored it to being a young liver at the most fundamental level—like an instruction book that is clear and properly organised again.— Prof. Haim Cohen, research leader
La Conversación del Hearth Otra perspectiva de la historia
So they made old cells young again. Is that what this means?
More precisely, they restored the organization of DNA in aged liver cells. The cells themselves didn't become young—but the way their genetic instructions were arranged and read did.
Why does that matter? Why not just keep people from aging in the first place?
Because aging has already happened to billions of people. If you can reverse it, even partially, that changes the conversation entirely. You're not just slowing decline anymore.
But it's mice. Doesn't that always mean we're decades away from human treatment?
Often, yes. But this is different because they've shown the mechanism works in already-aged tissue. That's the hard part. The translation to humans is still uncertain, but the principle is proven.
What would happen if this worked in human livers? Or brains?
That's the question everyone will be asking now. You'd potentially be able to restore function to organs that have deteriorated. But we don't know yet if SIRT6 can do this everywhere, or if there are limits.
Is this the beginning of something, or just a curiosity?
It's the beginning of something. It's the first time anyone has shown that a specific protein can actually reverse aging changes in already-aged animals. That's the threshold being crossed here.