Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents.
Level 5 - mechanism / opinion, no new human data
Bench, invertebrate (C. elegans), and rodent animal research.
PubMed 27400265 · doi:10.1038/nm.4132
What was done
Investigated the biological effects of urolithin A (a metabolite of ellagitannins found in pomegranates, nuts, and berries) in vitro and in vivo. The authors tested oral urolithin A in *Caenorhabditis elegans* for effects on mitophagy, mitochondrial accumulation, lifespan, mobility, pharyngeal pumping, and respiratory capacity. They also tested oral urolithin A on exercise capacity in two mouse models of age-related muscle decline and in young rats.
What was found
Urolithin A induced mitophagy in vitro and in vivo. In *C. elegans*, it prevented age-related accumulation of dysfunctional mitochondria, maintained mitochondrial respiratory capacity, prolonged lifespan, and preserved mobility and pharyngeal pumping. In rodents, oral urolithin A improved exercise capacity in both aged mouse models and young rats. The abstract reports no numerical values or effect sizes.
Why it matters
Identifies urolithin A as a dietary-derived metabolite capable of stimulating mitophagy, presenting a candidate mechanism and compound for targeting age-related mitochondrial and muscle decline.
Limits
All findings are preclinical in cell culture, nematodes, and rodents; human efficacy and safety were not tested. The abstract does not report sample sizes, specific dosages, treatment durations, or quantitative effect sizes.
Cited by
- supports Studies in cultured cells and animal models show that urolithin A improves mitochondrial quality.