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The role of JNK as an amplification pathway for mitochondrial damage induced by APAP has been extensively investigated using different approaches, from pharmacological inhibition to antisense oligonucleotides-mediated knockdown of Jnk1 and Jnk2 or global Jnk2 deletion in mice (Xie et al., 2015), highlighting the hierarchical relationship between ASK1 and JNK in APAP hepatotoxicity

Semi-targeted raw data from the Metabolon platform was similarly processed with our in-house script, performing corresponding normalization for biological material based on the total integrated peak area values of high-confidence metabolites

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