The Claim
Urolithin A activates PKGIα through oxidation at cysteine 42 in recombinant protein assays, rat vascular smooth muscle cells, and neonatal rat cardiomyocytes, demonstrating a conserved molecular mechanism across species and tissue types.
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.
Urolithin A causes a specific chemical change at cysteine 42 in the PKGIα protein, leading to its activation in laboratory protein systems, rat blood vessel cells, and rat heart cells.
See the scientific wording
Urolithin A activates PKGIα through oxidation at cysteine 42 in recombinant protein assays, rat vascular smooth muscle cells, and neonatal rat cardiomyocytes, demonstrating a conserved molecular mechanism across species and tissue types.
Urolithin A chemically modifies a specific spot on a protein called PKGIα, which turns the protein on. This activated protein then adds a phosphate group to another protein that controls calcium removal in heart and blood vessel cells. Faster calcium removal lets these cells relax more quickly, improving heart filling and blood vessel function.
What the research says
1 studyStudy: Targeting Cysteine 42 in PKGIa limits diastolic dysfunction in HFpEF
Urolithin A turns on a heart and blood vessel protein by tweaking a specific spot on it (cysteine 42), and this works the same way in rat cells and human heart tissue — but only if that spot isn't broken.
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.