Loss of farnesoid X receptor (FXR) exacerbated the ferroptosis signaling pathway by enhancing iron accumulation, increasing lipid peroxidation, decreasing GSH levels and reducing GPX4 expression in cisplatin-treated mice and HK-2 cells [175]
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Furthermore, periosteum bone formation rate and mineralizing surface also appeared to be preserved and several-fold higher than in catabolic agent-only models, partially restoring the suppressed bone formation
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