ScholarWorks@경상국립대학교

초록

Acetaminophen [N-acetyl-p-aminophenol (APAP)] overdose is a leading cause of acute liver failure worldwide, chiefly due to its hepatotoxic effects. The pathogenesis of APAP-induced acute liver injury (ALI) involves complex interactions among various hepatic cell types, each playing a distinct role in the progression of the injury. Hepatocytes, the primary targets of APAP toxicity, undergo oxidative stress, mitochondrial dysfunction, and necrosis following the formation of the toxic metabolite N-acetyl-p-benzoquinone imine. Additionally, other hepatic cells and infiltrating immune cells responding to liver injury significantly contribute to the pathogenesis of APAP-induced ALI. This review synthesizes current mechanistic insights to offer a detailed understanding of the specific contributions of hepatic cells to APAP-induced liver injury, emphasizing potential therapeutic targets designed to reduce liver damage and enhance patient outcomes. Additionally, it identifies potential therapeutic targets within these cellular pathways that could be leveraged to alleviate liver damage and enhance clinical outcomes for patients affected by APAP overdose.

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