For the millions who live with a form of heart failure that medicine has long struggled to address, a compound born from the digestion of pomegranates and walnuts may offer an unexpected opening. Researchers at King's College London have found that urolithin A, a naturally occurring molecule, can restore significant heart function in laboratory models of a condition where the heart stiffens rather than weakens — a distinction that has made it resistant to conventional therapies. The discovery is preliminary, but it arrives with an unusual advantage: the compound already has a human safety reco
Pomegranate Compound Shows 80% Heart Function Improvement in Hard-to-Treat Failure
Millions living with heart failure with preserved ejection fraction experience breathlessness, fatigue, reduced exercise ability, and poor quality of life due to limited treatment options.
A stiffened heart that cannot relax between beats
Mark
So this compound comes from eating pomegranates—does that mean people with this type of heart failure should start eating pomegranates now?
Mimi
The researchers are careful not to say that. The 80% improvement was measured in animal models and in engineered human tissue in the lab. That's not the same as giving the compound to actual patients and seeing if it works.
Luke
Right. And we should be clear about what "80% improvement" means here. It's a measure of heart function in controlled laboratory conditions. We don't know yet if that translates to the breathlessness and fatigue that patients actually experience.
Mimi
True. But the fact that it worked in engineered human tissue—not just animal models—does suggest there's something real here worth pursuing in human trials.
Mark
Why is this type of heart failure so hard to treat in the first place?
Mimi
Because it's not driven by a single cause. It's linked to aging, high blood pressure, diabetes, obesity—multiple factors working together. So there's no one drug target that fixes everything.
Luke
And half of all heart failure cases are this type. That's a huge population with limited options. Right now doctors just manage the underlying conditions and tell people to lose weight and control their blood sugar.
Mark
So if urolithin A actually works in humans, it would be the first drug specifically designed for this?
Mimi
Potentially, yes. That's why the researchers are excited. They've identified both a drug target—the PKGlα protein—and a naturally occurring compound that activates it.
Luke
But we need to be honest: we're still in the lab. The compound has a good safety record from previous human studies, which is encouraging. But nobody has tested it specifically for heart failure with preserved ejection fraction in actual patients yet.
Mark
What would the next step be?
Mimi
Clinical trials. You'd give the compound to patients with this condition and measure whether it actually improves their symptoms and their heart function over time.
Luke
And that takes years. So this is promising early-stage research, not a treatment people can access today.
Le Pouls
- Half of all heart failure cases belong to a form that leaves the heart too rigid to fill properly — and for which no targeted treatment currently exists, leaving patients to manage symptoms rather than address the disease itself.
- Millions endure daily breathlessness, fatigue, and shrinking physical capacity while medicine offers little beyond controlling contributing conditions like high blood pressure and diabetes.
- King's College London researchers found that urolithin A activates a key protein governing heart muscle relaxation, and in animal models it reversed dysfunction by up to 80% — also reducing scarring and abnormal muscle growth.
- The compound was then tested in engineered human heart tissue grown from stem cells, and it again improved relaxation, bringing the findings meaningfully closer to human relevance.
- Because urolithin A has already cleared human safety studies and exists naturally in common foods, the path toward clinical trials is shorter than it would be for an entirely novel drug.
- Scientists caution that eating pomegranates is not yet a prescription, but the research opens a credible avenue toward dietary or pharmaceutical interventions that could reshape how this disease is managed.
For the millions who live with a form of heart failure that medicine has long struggled to address, a compound born from the digestion of pomegranates and walnuts may offer an unexpected opening. Researchers at King's College London have found that urolithin A, a naturally occurring molecule, can restore significant heart function in laboratory models of a condition where the heart stiffens rather than weakens — a distinction that has made it resistant to conventional therapies. The discovery is preliminary, but it arrives with an unusual advantage: the compound already has a human safety record, shortening the distance between laboratory promise and clinical possibility.
Researchers at King's College London have identified a naturally occurring compound — urolithin A, produced in the body after eating pomegranates, walnuts, and certain berries — that restored heart function by up to 80% in laboratory models of one of cardiology's most treatment-resistant conditions.
The condition is heart failure with preserved ejection fraction, which accounts for roughly half of all heart failure cases. Unlike the more familiar form of heart failure, the heart here retains its pumping strength but loses its flexibility — stiffening so that it cannot properly relax and fill between beats. The consequences are real and grinding: breathlessness, fatigue, reduced ability to exercise, and a slow erosion of daily life. Doctors currently manage underlying causes like high blood pressure and diabetes, and recommend lifestyle changes, but no targeted pharmaceutical treatment reliably works.
The King's College team found that urolithin A activates a protein called PKGlα, which governs how heart muscle relaxes and how blood vessels function. In animal models, treated hearts relaxed more effectively, showed less fibrosis — the scarring that progressively stiffens cardiac tissue — and avoided the harmful enlargement of heart muscle cells typical of the disease. The researchers then tested the compound in engineered human heart tissue derived from stem cells, a model that closely mimics real cardiac muscle. The results held: tissue relaxation improved significantly, suggesting the findings could translate to living patients.
What distinguishes this discovery is that urolithin A is not an untested synthetic molecule. It has already been studied in humans and carries a favorable safety profile, and it arises naturally from foods people already consume. Senior author Dr. Joseph Burgoyne noted the potential to improve both clinical outcomes and quality of life for millions — while being careful to clarify that the evidence does not yet support eating pomegranates as treatment. Human clinical trials remain the necessary next step. The research, funded by the British Heart Foundation, points toward a future where dietary strategies or urolithin A-based therapies might finally offer this underserved patient population something medicine has not yet been able to provide.
Researchers at King's College London have identified a compound that emerges naturally in the body after eating pomegranates, walnuts, and certain berries—and in laboratory tests, it restored heart function by up to 80% in a form of heart failure that has long resisted treatment.
The compound is urolithin A, and the discovery matters because it targets a type of heart failure that accounts for roughly half of all heart failure cases but remains stubbornly difficult to manage. In this condition, called heart failure with preserved ejection fraction, the heart retains its ability to pump blood but loses its flexibility. The muscle stiffens, making it harder for the heart to relax and fill between beats. The result is breathlessness, fatigue, a diminished capacity for exercise, and a steady erosion of quality of life. Current treatment is limited—doctors typically manage the underlying causes like high blood pressure, diabetes, and aging, while recommending lifestyle changes such as weight loss and blood sugar control. There is no targeted pharmaceutical intervention that reliably works.
The King's College team discovered that urolithin A activates a protein called PKGlα, which plays a central role in how blood vessels function and how heart muscle relaxes. When the researchers tested the compound in animal models of the disease, treated hearts showed marked improvement in their ability to relax. The tissue also showed less scarring, a process called fibrosis that stiffens the heart over time. The compound also prevented the harmful enlargement of heart muscle cells that typically occurs in this condition. To move closer to human application, the scientists then tested urolithin A in engineered human heart tissue grown from stem cells—a laboratory model that closely approximates the structure and behavior of actual cardiac muscle. Again, the compound significantly improved tissue relaxation, suggesting the laboratory findings might translate to living patients.
What makes this discovery particularly promising is that urolithin A is not some novel synthetic molecule being tested for the first time in humans. The compound has already been evaluated in human studies and has shown a favorable safety profile. It is also naturally present in foods that people already eat. This combination—a naturally derived compound with an established safety record and a clear mechanism of action in human tissue—creates a genuine pathway toward a new treatment.
Dr. Joseph Burgoyne, the senior author, noted that the findings raise the possibility of developing treatments that could improve both clinical outcomes and quality of life for millions living with this form of heart failure. He was careful to note, however, that the evidence does not yet support telling people to eat pomegranates as a treatment. The laboratory work is compelling, but human clinical trials remain necessary. What the research does suggest is that dietary approaches that boost urolithin A production might eventually help alleviate the condition—a possibility that would represent a meaningful shift in how this disease is managed. The study was funded by the British Heart Foundation.
Citations marquantes
These findings raise the possibility that dietary approaches that enhance urolithin A production may help alleviate this condition.— Dr. Joseph Burgoyne, King's College London
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