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Although the exact molecular mechanism of the dual regulation of ferroptosis by butyrate has not been fully elucidated, accumulating experimental evidence gradually suggests that it may be involved in the pathophysiological regulation of OA by regulating the ferroptosis process of chondrocytes

These reactive astrocytes exhibit altered behaviors that can both support and disrupt neuronal function, creating a complex environment that accelerates neurodegeneration

Mice fed a diet deficient in selenium resulted in fibrocartilage formation at the articular surface, ultimately showing degeneration of articular cartilage 63

This enables them to confer their functional properties directly on the brain [146]

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