Urolithin A provides cardioprotection and mitochondrial quality enhancement preclinically and improves human cardiovascular health biomarkers.
Level 3 - non-randomized controlled study
Mixed preclinical research with a non-randomized or unspecified human interventional trial evaluating surrogate biomarkers
PubMed 40034121 · doi:10.1016/j.isci.2025.111814
What was done
Researchers evaluated mitochondrial quality dysfunctions in human cardiomyocytes during aging and chronic disease. They tested the mitophagy activator urolithin A (UA) in preclinical models of natural aging and heart failure to measure systolic and diastolic function, mitochondrial ultrastructure, and mitophagy. They also administered UA to healthy older adults for 4 months to measure changes in plasma ceramides linked to cardiovascular disease risk.
What was found
No quantitative data, sample sizes, or p-values were reported in the abstract. Preclinically, UA reduced systolic and diastolic cardiac dysfunction and restored mitochondrial ultrastructural defects and mitophagy. In healthy older adults, 4 months of UA supplementation significantly reduced plasma ceramides.
Why it matters
This study provides translational evidence that urolithin A can enhance mitochondrial quality in cardiac models and reduce plasma ceramide biomarkers associated with cardiovascular risk in aging humans.
Limits
The abstract provides no sample sizes for the preclinical or human cohorts. Details regarding the human trial design (randomization, blinding, control group, and dosing) are entirely omitted. Human findings are limited to surrogate plasma biomarkers rather than functional cardiac or clinical outcomes.
Cited by
- supports In animal models of heart failure, Mitopure (Urolithin A) supplementation reversed cardiac damage by improving mitochondrial health.
- supports In clinical trials, Mitopure supplementation reduces plasma levels of ceramides in humans.