LONDON / RankWire.AI / – A naturally occurring compound associated with pomegranates has demonstrated improvements in multiple heart function indicators within experimental models of HFpEF. Urolithin A, the compound in question, enhanced the heart’s ability to relax more efficiently between beats. Additionally, it decreased fibrosis and prevented abnormal enlargement of cardiac muscle cells. Some parameters showed increases of up to 80% compared to untreated animal models. Researchers also observed positive effects in engineered human cardiac tissue, adding further evidence from laboratory studies to these findings.
HFpEF, or heart failure with preserved ejection fraction, arises when the heart continues to pump normally but loses its ability to relax properly. This impairs how the chambers fill with blood during the relaxation phase, leading to symptoms such as breathlessness, fatigue, and diminished exercise capacity. The condition accounts for nearly half of all heart failure cases in the United Kingdom. Urolithin A forms when gut microbes metabolize certain compounds present in pomegranates, walnuts, and various berries. However, its production varies among individuals.
The researchers identified PKGIα, a protein instrumental in maintaining normal blood vessel function and facilitating heart muscle relaxation, as the target of urolithin A. The compound modifies a specific segment of the protein, known as cysteine 42, which activates a pathway associated with cardiovascular health. The study also assessed the influence of urolithin A on heart tissue architecture. King’s College London researchers reported improved diastolic function, less tissue scarring, and a reduction in the enlargement of heart muscle cells in the experimental models treated with the compound.
Laboratory models showed enhanced cardiac relaxation following urolithin A administration
The animal studies concentrated on diastolic function, which measures the heart’s capacity to relax and fill with blood after each contraction. The models treated with urolithin A exhibited superior performance across various parameters compared to untreated controls. The research also noted decreased fibrosis levels, which can stiffen heart tissue and hinder proper filling. The reported improvements of up to 80% applied to specific experimental measurements. It is important to emphasize that these findings do not equate to an 80% enhancement in patient outcomes, and the research did not involve clinical trials with humans.
Furthermore, urolithin A was tested in engineered human heart tissues derived from stem cells. These models enable scientists to study human cardiac tissue in controlled laboratory settings. In these tests, the compound improved both relaxation and contraction dynamics. Prior human studies exploring urolithin A for different applications have indicated a favorable safety profile. Nonetheless, this new research on heart failure was conducted exclusively on animal models and laboratory-engineered tissues, with no trials involving actual patients with HFpEF.
Further human clinical trials are necessary to confirm potential benefits for heart failure
British Heart Foundation funded this investigation and highlighted urolithin A’s promising effect on heart relaxation during early testing phases. The organization also clarified that these results do not constitute proof of a treatment for HFpEF. Researchers warned against interpreting the findings as evidence that consuming pomegranates could treat heart failure. The study focused on urolithin A’s biological activity, not on dietary pomegranate intake. No tested foods demonstrated the ability to prevent or cure heart failure in this research.
This research pinpoints PKGIα cysteine 42 as a specific biological target relevant to HFpEF. It also offers laboratory evidence that urolithin A activates this pathway, leading to improvements in various markers associated with cardiac relaxation. HFpEF frequently coexists with conditions such as high blood pressure, obesity, and diabetes. It remains a significant form of heart failure globally. To establish whether urolithin A produces similar effects in humans and whether these effects translate into meaningful health improvements, clinical trials are essential.
}#