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Rotenone treatment significantly reduced survival compared to untreated controls, confirming that mitochondrial respiration is a critical mediator of cholesterol-induced hepatic reprogramming and host defense ( Fig

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Neither tested dose reduction protocols

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Intracellular glutathione also followed the trend of GCLC, exhibiting an NFT-dependent increase that was reversed by anti Nrf2-siRNA to levels comparable to those observed in untreated HepG2 cells (Fig