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Within the metabolic reprogramming and ferroptosis mechanisms discussed earlier, these immune cells and inflammatory mediators modulate iron homeostasis and lipid peroxidation, among other metabolic pathways

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In this regard, using broad-spectrum PKC inhibitors, it has been shown that PKC blockade upregulated p-AMPK levels, resulting in increased levels of LC3-II formation and p62 degradation indicative of increased autophagy, which resulted in the protection against APAP hepatotoxicity (Saberi et al., 2014), thus complementing the JNK-dependent contribution of PKC in APAP hepatotoxicity described above

Targeting p53 presents a substantial risk of off-target effects

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