A compound associated with eating pomegranates could have a notable impact on your heart health, scientists at King's College, London, have recently found. The researchers discovered that urolithin A—which is produced in the body after consuming foods such as pomegranates, walnuts and some berries—could improve heart function by up to 80 percent among those who suffer from a type of heart failure that currently has limited treatment options. Urolithin A was found to improve the heart’s ability to relax, reduce scarring and prevent harmful enlargement of the heart, which is particularly notable for those who are experiencing heart failure with preserved ejection fraction.
The condition accounts for around half of all heart failure cases and occurs when the heart retains its ability to pump blood but becomes stiff and less able to relax between beats, making it harder to fill with blood. It can lead to breathlessness, fatigue, reduced ability to exercise and an overall poorer quality of life. "This type of heart failure is becoming increasingly common as populations age and rates of obesity and diabetes rise.
Despite its growing burden, treatment options remain limited because the disease is complex and varies considerably between patients," Dr. Joseph Burgoyne, senior author of the study and scientist at King’s College London, said. The study was published in the journal Science Advances last month.
Urolithin A is "produced by bacteria in our gut when they metabolize compounds called ellagitannins, which are found in pomegranates, walnuts and some berries," Burgoyne told Newsweek, clarifying that while the compound is found in pomegranates, it is not in significant amounts. He also said eating a particular amount of pomegranate is not equivalent to receiving a defined dose of urolithin A. Burgoyne said the team found urolithin A activated a protein called PKGIα, which "plays an important role in helping the heart muscle and blood vessels relax." "It does this by directly modifying a specific amino acid on the protein, cysteine 42," he said.
"In heart muscle cells, this ultimately improves the handling of calcium, allowing the muscle to relax more effectively between beats." This is particularly relevant to heart failure with preserved ejection fraction because, although the condition means the heart can still contract reasonably normally, it "becomes stiff and has difficulty relaxing and filling with blood," Burgoyne said. In the animal-based model, urolithin A "improved measures of cardiac relaxation, reduced fibrosis or scarring, reduced enlargement of heart muscle cells and improved exercise capacity," he added. "We also saw faster relaxation in engineered human heart tissue." Burgoyne said he believed the "most important aspect of the study is that we have identified a new biological mechanism that could potentially be targeted therapeutically." This is particularly notable as heart failure with preserved ejection fraction is especially challenging to treat because it is driven by several interacting processes, including aging, high blood pressure, obesity and diabetes.
However, he said the results suggest that targeting cysteine 42 on PKGIα could "directly improve" one of the fundamental problems in the condition—the inability of the heart to relax properly, while also reducing some of the structural changes such as scarring and cardiac hypertrophy (enlargement of the heart). He also said that urolithin A has previously been found to have a "favorable safety profile, which supports the feasibility of evaluating it in a clinical trial in patients with heart failure." Jie Su et al. (2026) Targeting PKGIα Cys42 attenuates cardiac dysfunction in heart failure with preserved ejection fraction. DOI:10.1126/sciadv.aec8088 Contact Newsweek editors on this story: Kara Dolman and Tony Phillips.
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