The Claim
The cardioprotective effect of urolithin A in mice with HFpEF is dependent on cysteine 42 of PKGIα, as this effect is abolished in C42S PKGIα knock-in mice.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In mice with heart failure with preserved ejection fraction, urolithin A protects the heart only if the protein PKGIα has cysteine at position 42; replacing this amino acid eliminates the protective effect.
See the scientific wording
The cardioprotective effect of urolithin A in HFpEF mice is abolished in C42S PKGIα knock-in mice, confirming that cysteine 42 is necessary for its functional benefit.
Urolithin A changes a specific spot on a heart protein, which turns the protein on. This activated protein then signals another protein to remove calcium from heart muscle cells faster. Faster calcium removal lets the heart muscle relax more completely between beats, which improves the heart's ability to fill with blood.
What the research says
1 studyStudy: Targeting Cysteine 42 in PKGIa limits diastolic dysfunction in HFpEF
When scientists changed a tiny part of a heart protein in mice, urolithin A stopped helping the heart relax — proving that this specific part is needed for the medicine to work.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.