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177 Further mechanistic studies showed that GPX4 and SLC7A11 levels decreased in the number of endplate chondrocytes of an iron overload model in an FAC dose-dependent manner, while the expression of lipid peroxides (4-HNE) increased, accompanied by a markedly increase in the number of condensed mitochondria, suggesting that excessive iron promoted endplate chondrocyte mitochondrial dysfunction and ferroptosis
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