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While the molecular mechanisms of APAP hepatotoxicity are diverse and include different players, including innate immune response, in this review we will focus on the mitochondrial–lysosomal axis, which has emerged as a novel liason in several pathologies, including lysosomal storage diseases ( APAP Metabolism: Mitochondrial Targeting Acetaminophen hepatoxicity is caused by the action of a reactive metabolite derived from APAP metabolism in the liver that ultimately targets mitochondrial components resulting in impaired mitochondrial function

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Most of the research began in rodents, and much of the practical experience comes from human clinical use