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Through directed differentiation, these cells can be induced to transform into osteoblasts, chondrocytes, and adipocytes, offering new therapeutic avenues for the repair of bone injuries, degenerative diseases, and congenital defects

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In conclusion, we show that APAP toxicity in HepG2 cells is largely independent of oxidative stress, and is linked instead to a decoupling of glycolysis from the TCA cycle, lactic acidosis, reduced NADPH production, and subsequent suppression of the anabolic pathways required for rapid growth

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