Tier 3 — preclinical

Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis

D'Amico D, Olmer M, Fouassier AM, Valdés P, Andreux PA, Rinsch C, Lotz M
Aging Cell 2022 21(8):e13662

Bibliography

PubMed
PMID 35778837
PubMed Central
PMC9381911
Competing interests
D'Amico, Fouassier and Rinsch were Amazentis employees; Valdés and Andreux were prior Amazentis employees; Rinsch was also a board member.

Study snapshot

DesignTranslational preclinical study using human primary chondrocytes and a mouse osteoarthritis model
ModelHuman cartilage cells from healthy donors and osteoarthritis patients; mouse osteoarthritis model
SampleMultiple human-cell donor samples and animal cohorts
InterventionUrolithin A / Mitopure in cell culture and experimental mouse treatment
DurationVaried by experimental model
EndpointsChondrocyte mitophagy and mitochondrial respiration; Cartilage degeneration; Synovial inflammation; Pain-related behavior; Joint mitochondrial content

What the study showed, in plain terms

This study linked Urolithin A's mitophagy mechanism to joint aging. It improved mitochondrial function in cartilage cells from both healthy donors and people with osteoarthritis, and in mice it reduced cartilage degeneration, synovial inflammation and pain. The clinically important limitation is that the outcome data are still preclinical.

Key findings

Urolithin A increased mitophagy and mitochondrial respiration in primary human chondrocytes.

Mouse osteoarthritis progression, cartilage damage, synovial inflammation and pain were reduced.

Joint mitochondrial content increased alongside the structural changes.

What this study can and cannot tell us

No osteoarthritis patient was treated with oral Urolithin A in this study.

Mouse joint outcomes cannot establish symptom relief or disease modification in humans.

The study included substantial Amazentis involvement.

Editorial review

Reviewed by the Biohack Blueprint research team

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