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5, SeNPs exert their anti-ferroptotic effects in renal tubular epithelial cells through a stepwise mechanism: they are first internalized into the cytoplasm via endocytosis, subsequently enriched within lysosomes, and then stimulate XBP1 expression to block I/R-induced excessive activation of NCOA4-mediated ferritinophagy, ultimately interrupting iron-dependent cell death cascades

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In OA, defects in mitochondrial biogenesis can promote pro-catabolic responses, while maintaining this process is crucial for chondrocyte homeostasis, making it a potential target for early OA intervention (29)