Tier 3 — preclinical

Urolithin A improves myocardial ischemia-reperfusion injury by attenuating oxidative stress and ferroptosis through Nrf2 pathway

Su Z, Li P, Ding W, Gao Y
International Immunopharmacology 2024 143(Pt 2):113394

Bibliography

PubMed
PMID 39437484
DOI
10.1016/j.intimp.2024.113394
Competing interests
The authors declared no known competing financial interests or personal relationships.

Study snapshot

DesignMouse myocardial ischemia/reperfusion model plus cardiomyocyte hypoxia/reoxygenation experiments
ModelC57BL mice and cardiac-cell models
SampleMultiple preclinical cohorts
InterventionUrolithin A with Nrf2 pathway inhibition experiments
DurationAcute experimental injury model
EndpointsInfarct injury and cardiac function; Oxidative stress; Mitochondrial damage; Ferroptosis; Nrf2 signaling

What the study showed, in plain terms

In a mouse/cell myocardial ischemia-reperfusion model, Urolithin A reduced oxidative stress, mitochondrial damage and ferroptosis and improved cardiac injury measures through Nrf2-dependent signaling. It supports cardiovascular mechanism content, not a claim that Urolithin A treats heart attacks in humans.

Key findings

Cardiac injury and function improved in experimental I/R models.

Oxidative stress, mitochondrial damage and ferroptosis were reduced.

Nrf2 activation was required for much of the protective effect.

What this study can and cannot tell us

No human cardiovascular trial was performed.

Acute ischemia/reperfusion models do not establish chronic cardiovascular prevention.

Therapeutic experimental dosing cannot be transferred directly to supplements.

Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology