A natural compound produced in the human body after eating pomegranates improves heart muscle relaxation and reduces tissue scarring in preclinical models of a hard-to-treat form of heart failure, according to a study published by researchers at King’s College London.
Understanding Preserved Ejection Fraction Heart Failure
Heart failure with preserved ejection fraction occurs when the heart muscle contracts normally but becomes stiff and fails to relax properly between beats. This stiffness prevents the chambers from filling adequately with blood, leading to symptoms such as chronic fatigue, severe breathlessness, and a severely limited ability to exercise. According to King’s College London researchers, the condition accounts for approximately half of all heart failure cases and is increasingly prevalent due to aging populations and rising rates of obesity and diabetes. Because the heart retains its normal pumping strength, standard heart failure therapies prove largely ineffective, forcing clinicians to focus instead on managing underlying drivers like hypertension and blood sugar levels.
How Urolithin A Targets Stiff Heart Tissue
The experimental compound investigated in the study is urolithin A, a metabolite produced when gut bacteria break down ellagitannins found in foods such as pomegranates, walnuts, and certain berries. While urolithin A has previously gained scientific attention for its role in supporting mitochondrial health and cellular energy production during aging, the King’s College London team identified an entirely new mechanism of action. According to the study’s senior author, Dr. Joseph Burgoyne, scientists discovered that urolithin A directly activates a critical protein called PKG1α. This specific protein regulates both blood vessel tone and heart muscle relaxation. When urolithin A targets a specific amino acid on PKG1α, it triggers a protective pathway that enhances cardiovascular function.
Preclinical Results and Human Stem Cell Tests
In controlled laboratory experiments using animal models, treatment with urolithin A improved overall measures of heart function compared to untreated controls. Further microscopic analysis revealed that the compound successfully reduced cardiac fibrosis, which is the accumulation of excess scar tissue that stiffens the heart walls, and prevented harmful enlargement of individual heart muscle cells. To evaluate whether these laboratory benefits could translate to humans, the researchers tested urolithin A on engineered human heart tissue created from stem cells. This advanced cellular model mimics the structure and mechanics of human cardiac muscle. The tests confirmed that urolithin A significantly improved tissue relaxation in the human-derived cells. Furthermore, because urolithin A has already undergone preliminary human safety evaluations in separate nutritional and aging studies, it possesses a well-documented safety profile, though researchers emphasize that clinical trials specifically targeting heart failure patients are still required.
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