A liver-cartilage selenium axis underlies metabolic comorbidity in osteoarthritis.

Hepatic dysfunction disrupts selenium delivery to cartilage, promoting osteoarthritis in mice and humans, with a 20% higher OA prevalence among individuals with liver disease.

• Why it matters: Metabolic dysfunction is increasingly recognized as a key contributor to osteoarthritis, but the underlying systemic mechanisms remain unclear, limiting targeted prevention strategies.
• What they did: The study examined nationwide cohorts and murine models of liver injury, revealing that hepatic stress impairs the selenoprotein P-ApoER2 axis, reducing selenium supply to cartilage and promoting chondrocyte senescence.
• The result: Inorganic selenium supplementation restores cartilage selenoproteins and alleviates osteoarthritis, suggesting selenium as a modifiable nutritional factor for preventing joint comorbidity in metabolic liver disease.