LONDON / RankWire.AI / – A compound naturally derived from pomegranates has demonstrated the ability to improve several key indicators of cardiac performance in experimental models of HFpEF. The substance, urolithin A, facilitated more effective relaxation of the heart between beats and also decreased fibrosis as well as abnormal enlargement of heart muscle cells. Some parameters showed improvements of up to 80% compared to untreated animal subjects. Researchers further confirmed these benefits in engineered human heart tissue, providing additional in-lab support for the findings.
HFpEF, or heart failure with preserved ejection fraction, occurs when the heart retains its ability to pump blood normally but struggles to relax properly. This impairs the chambers’ ability to fill with blood during relaxation phases, often resulting in symptoms such as breathlessness, fatigue, and diminished exercise tolerance. In the United Kingdom, HFpEF accounts for approximately fifty percent of all heart failure cases. Urolithin A is produced when gut bacteria process certain compounds present in pomegranates, walnuts, and various berries, although individual production levels can vary from person to person.
The researchers identified PKGIα, a protein essential for proper blood vessel function and heart muscle relaxation, as the target of urolithin A. The compound modifies a specific site on this protein called cysteine 42, which triggers a pathway associated with cardiovascular health. Additionally, the study explored how urolithin A influenced heart tissue structure. King’s College London investigators observed enhanced diastolic function, decreased tissue scarring, and reduced hypertrophy of cardiac muscle cells in the experimental models treated with the compound.
Laboratory models showed improved heart relaxation with urolithin A
The animal studies focused on diastolic performance, which gauges how well the heart relaxes and fills after each beat. Models treated with urolithin A displayed superior results across multiple metrics compared to untreated controls. The research also noted reduced fibrosis, which can stiffen heart tissue and hinder filling. The maximum reported improvement of 80% was specific to selected experimental parameters and does not imply that patients would experience an equivalent benefit. The study did not assess clinical outcomes in humans.
Furthermore, urolithin A was tested on engineered human heart tissue derived from stem cells. These models provide a controlled environment for studying human cardiac tissue. The compound enhanced both relaxation and contraction behaviors in these samples. Prior studies involving urolithin A in humans for other purposes have shown a favorable safety profile. However, the current research into HFpEF did not involve human patients, so findings are limited to animal models and lab-grown tissue.
Further human clinical trials are necessary to confirm heart failure benefits
The British Heart Foundation funded the investigation and emphasized the compound’s impact on heart relaxation observed in early-stage testing. The organization clarified that these results do not constitute a proven treatment for HFpEF. Researchers also warned against interpreting the findings as evidence that consuming pomegranates could treat heart failure. The research centered on urolithin A’s biological activity, not dietary intake of pomegranates. No foods examined in the study demonstrated an ability to prevent or cure heart failure.
This research pinpointed PKGIα cysteine 42 as a specific molecular target relevant to HFpEF. It also offers laboratory evidence that urolithin A can activate this pathway and positively influence several markers of cardiac relaxation. HFpEF commonly coexists with high blood pressure, obesity, and diabetes, and remains a significant form of heart failure worldwide. To determine if these promising effects translate into human health benefits, clinical trials are essential to evaluate whether the compound produces similar outcomes in patients.