In brief

The study identifies a direct action on PKGIα and reports favourable signals in engineered human heart tissue, including improved relaxation and contraction kinetics.

Researchers screened natural compounds for the ability to modulate cysteine 42 in PKGIα, a kinase involved in vascular and diastolic relaxation. Urolithin A emerged as a direct activator of this mechanism.

In a multihit model of heart failure with preserved ejection fraction, treatment improved diastolic function and attenuated fibrosis, hypertrophy and remodelling. The effect depended on Cys42, strengthening the mechanistic interpretation.

Engineered human heart tissue also showed more favourable relaxation and contraction kinetics. This remains an early translational step: pharmacokinetics, safety and clinical trials are needed before any cardiovascular benefit in humans can be claimed.

Why it matters

For ingredient development, the result extends urolithin A from healthy ageing and muscle function towards cardiovascular healthy ageing.

Evidence limit

A preclinical study in animal models and engineered tissue. It does not establish cardiovascular efficacy, an effective dose or supplementation safety in people with HFpEF.

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Read the original source · Science Advances / PubMed