The Claim

Urolithin A induces PKGIα-dependent phosphorylation of phospholamban in neonatal rat ventricular myocytes.

Source: Targeting Cysteine 42 in PKGIa limits diastolic dysfunction in HFpEF

What the research says

Supports is higher

Support is ahead, but a single strong opposing study can change this.

Supports
55score
Challenges
0score

These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.

How it works
1 study reviewed
In plain English

Urolithin A triggers a specific biochemical change in heart muscle cells from newborn rats, involving the phosphorylation of phospholamban through the PKGIα pathway.

See the scientific wording

Urolithin A induces PKGIα-dependent phosphorylation of phospholamban in neonatal rat ventricular myocytes, suggesting a downstream mechanism for improved cardiac relaxation.

Why this might work

Urolithin A triggers a chemical change in a heart protein called PKGIα, which turns it on. This activated protein then adds a phosphate group to another protein called phospholamban, which lets the heart muscle pump calcium back into storage faster. This speeds up the relaxation of the heart muscle after each beat.

Verified mechanismbased on 1 study

What the research says

1 study

  1. Study: Targeting Cysteine 42 in PKGIa limits diastolic dysfunction in HFpEF

    Urolithin A helps heart cells relax better by turning on a specific protein (PKGIα), which then tweaks another protein (phospholamban) that controls heart relaxation — and this was proven in both rat and human heart tissue.

Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies

Fit Body Science verdict — we translate health claims into clear verdicts backed by peer-reviewed research.

Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.