Longevity & AgingPress Release

Pomegranate Compound Urolithin A Boosts Heart Function by 80% in Heart Failure Models

Urolithin A, produced after eating pomegranates and walnuts, improved heart relaxation and reduced scarring by up to 80% in animal and human tissue models.

Tuesday, September 29, 2026 1 view
Published in ScienceDaily Aging
Article visualization: Pomegranate Compound Urolithin A Boosts Heart Function by 80% in Heart Failure Models

Summary

Researchers at King's College London found that urolithin A, a compound the body makes after consuming pomegranates, walnuts, and certain berries, dramatically improved heart function in experimental models of heart failure with preserved ejection fraction. This hard-to-treat condition, affecting nearly half of all heart failure patients, causes the heart to become too stiff to relax properly between beats. Urolithin A worked by activating a protein called PKGlα, which governs heart muscle relaxation and blood vessel function. In animal models, heart function improved by up to 80%. The compound also reduced fibrosis and abnormal cell enlargement. Crucially, it also improved relaxation in engineered human heart tissue derived from stem cells, strengthening the case for human relevance.

Detailed Summary

Heart failure with preserved ejection fraction is one of cardiology's most frustrating challenges. The heart still pumps blood adequately, but stiffened muscle prevents proper filling between beats, causing breathlessness, fatigue, and reduced exercise capacity. It accounts for roughly half of all heart failure cases and is closely linked to aging, obesity, high blood pressure, and diabetes — yet treatment options remain thin.

Researchers at King's College London now report that urolithin A, a compound produced in the gut after eating pomegranates, walnuts, and certain berries, may offer a new therapeutic angle. The study is the first to show that urolithin A activates PKGlα, a protein critical to heart muscle relaxation and vascular function, by targeting a specific amino acid within it. This triggers a cardiovascular-protective signaling pathway.

In animal models of the condition, urolithin A improved key measures of heart function by up to 80% compared with untreated controls. The compound also reduced fibrosis — the harmful scarring that stiffens heart tissue — and limited abnormal enlargement of heart muscle cells, helping them maintain more normal architecture and function.

The team then tested urolithin A in engineered human heart tissue built from stem cells, a model that closely mimics real cardiac muscle. Urolithin A significantly improved relaxation in this tissue, providing an important bridge toward human applicability and reinforcing the mechanistic findings from animal work.

Caveats are substantial. This remains preclinical research; no human clinical trials have been reported yet. Dietary intake of pomegranates produces highly variable urolithin A levels depending on individual gut microbiome composition. The 80% improvement figure comes from animal models, and translation to humans will require rigorous trials. Nonetheless, the dual action — improving relaxation while reducing scarring — makes urolithin A a compelling candidate for a condition that desperately needs new therapies.

Key Findings

  • Urolithin A improved heart function measures by up to 80% in animal models of heart failure with preserved ejection fraction.
  • The compound activates PKGlα protein, triggering a pathway that promotes heart muscle relaxation and vascular health.
  • Urolithin A reduced cardiac fibrosis and limited abnormal heart muscle cell enlargement in experimental models.
  • Urolithin A improved relaxation in engineered human heart tissue derived from stem cells, suggesting human relevance.
  • Heart failure with preserved ejection fraction affects ~half of all heart failure patients and is strongly linked to aging and metabolic disease.

Methodology

This is a news summary of primary preclinical research from King's College London, a highly credible research institution. Evidence derives from animal models and engineered human heart tissue created from stem cells; no human clinical trial data are reported. The article does not cite a specific journal, so the full peer-review status and methodology details should be verified against the primary publication.

Study Limitations

All functional improvement data come from animal models and lab-engineered tissue, not human patients, limiting direct clinical translation. Individual gut microbiome composition strongly determines how much urolithin A is produced from dietary precursors, so food-based strategies may have inconsistent effects. The primary journal article, specific animal model used, and full statistical details are not disclosed in this news summary and should be reviewed before drawing firm conclusions.

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