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Mitochondrial Dysfunction Drives Bone and Joint Disease — and Can Be ReversedRegenerative Medicine

Mitochondrial Dysfunction Drives Bone and Joint Disease — and Can Be Reversed

Osteoporosis, osteoarthritis, and rheumatoid arthritis are among the most common age-related conditions, and this review argues they share a single root mechanism: mitochondrial dysfunction. When mitochondria fail in bone, cartilage, and muscle cells, the consequences cascade — poor energy production, oxidative stress, faulty waste clearance, and inflammatory signals called mtDAMPs. The good news is that these defects appear reversible. Researchers catalog a growing toolkit of mitochondria-targeted interventions, including the antioxidants MitoQ and SkQ1, metabolic modulators like metformin and NAD+ boosters, the mitophagy inducer urolithin A, the fission inhibitor Mdivi-1, senolytic agents, and even experimental mitochondrial transplantation. The review closes by proposing a precision medicine approach that matches specific mitochondrial abnormalities to mechanism-based treatments, moving musculoskeletal medicine beyond symptom management toward genuine disease modification.

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