Overview
- This week researchers at King’s College London published a peer‑reviewed study showing that urolithin A activates the heart protein PKGIα by chemically modifying its Cys42 site.
- In mice with experimentally induced heart failure with preserved ejection fraction (HFpEF), a short course of urolithin A improved measures of diastolic relaxation, reduced fibrosis and chamber enlargement, and raised exercise activity.
- The benefits depended on the Cys42 residue because genetically modified mice lacking that site did not improve, providing a clear molecular mechanism for the effect.
- Urolithin A also sped contraction and relaxation in engineered human heart tissue grown from stem cells, suggesting translational relevance but not proving benefit in patients.
- Urolithin A is made by gut bacteria from ellagitannins in foods like pomegranates, berries and walnuts, yet experts warn individual microbiomes vary and human clinical trials are needed before any treatment or dietary guidance is recommended.