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Excessive oxidative stress and iron dependence are hallmark features of ferroptosis, in which high levels of ROS generation impair important components of the organism
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To achieve GSH depletion in liver, we engineered an adeno-associated virus (AAV) vector encoding Chac1 fused to a Myc tag, driven by the thyroxine-binding globulin (TBG) promoter to achieve liver-specific overexpression of Chac1 (Figure 1B)
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