Open AccessUrolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis
Author(s) -
D'Amico Davide,
Olmer Merissa,
Fouassier Andréane M.,
Valdés Pamela,
Andreux Pénélope A.,
Rinsch Chris,
Lotz Martin
Publication year - 2022
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.13662
Subject(s) - mitophagy , osteoarthritis , cartilage , mitochondrion , degeneration (medical) , inflammation , biology , disease , medicine , bioinformatics , pharmacology , pathology , autophagy , microbiology and biotechnology , anatomy , biochemistry , apoptosis , alternative medicine
Osteoarthritis (OA) is the most common age‐related joint disorder with no effective therapy. According to the World Health Organization, OA affects over 500 million people and is characterized by degradation of cartilage and other joint tissues, severe pain, and impaired mobility. Mitochondrial dysfunction contributes to OA pathology. However, interventions to rescue mitochondrial defects in human OA are not available. Urolithin A (Mitopure) is a natural postbiotic compound that promotes mitophagy and mitochondrial function and beneficially impacts muscle health in preclinical models of aging and in elderly and middle‐aged humans. Here, we showed that Urolithin A improved mitophagy and mitochondrial respiration in primary chondrocytes from joints of both healthy donors and OA patients. Furthermore, Urolithin A reduced disease progression in a mouse model of OA, decreasing cartilage degeneration, synovial inflammation, and pain. These improvements were associated with increased mitophagy and mitochondrial content, in joints of OA mice. These findings indicate that UA promotes joint mitochondrial health, alleviates OA pathology, and supports Urolithin A's potential to improve mobility with beneficial effects on structural damage in joints.