A natural compound found in fruits and nuts, known as urolithin A, may help reverse heart damage associated with a specific type of heart failure, according to recent research. Urolithin A is produced by gut bacteria that break down plant polyphenols present in foods like pomegranates, walnuts, and berries.
The compound is recognized for promoting cell health by clearing damaged cellular components and supporting muscle function, contributing to healthy aging. It is also available as a dietary supplement.
Scientists are investigating urolithin A's potential to treat heart failure with preserved ejection fraction (HFpEF), a condition affecting nearly half of the approximately 6.7 million American adults diagnosed with heart failure. In HFpEF, the heart's ability to relax and fill with blood between beats is impaired, even though its contraction function remains normal. This stiffness leads to symptoms such as shortness of breath and fatigue.
Promising Findings in Preclinical Studies
A study published in the journal Science Advances explored urolithin A's effects in mice. Researchers observed that the compound activates a heart protein, PKGIα, which plays a role in regulating the relaxation of the heart and blood vessels. By targeting a specific site on this protein, urolithin A appeared to enhance the heart's flexibility and mitigate damage caused by prolonged stiffness. The compound also reversed key characteristics of experimentally induced HFpEF in the mice.
Further experiments were conducted using engineered human heart tissue grown from stem cells in a laboratory. The treated human tissue demonstrated improved contraction and relaxation efficiency, suggesting that the benefits of urolithin A may extend to humans.
Historically, HFpEF has presented treatment challenges because many existing heart failure medications are designed to enhance pumping ability, which is not the primary issue in HFpEF. The condition's core problem lies in the heart's reduced ability to relax and fill adequately.
While these findings are currently limited to animal models and laboratory-grown human tissues, they suggest a novel therapeutic avenue that targets the underlying mechanisms of HFpEF. If future human trials yield similar results, urolithin A could offer a new treatment option for individuals living with this challenging condition.