Acetaminophen (APAP) overdose represents the most frequent cause of acute liver failure, resulting in death or liver transplantation in more than one third of patients in the United States. The effectiveness of the only antidote, N‐acetylcysteine, declines rapidly after APAP ingestion, long before patients are admitted to the clinic with symptoms of severe liver injury. The direct hepatotoxicity of APAP triggers a cascade of innate immune responses that may exacerbate or limit the progression of tissue damage. A better understanding of this complex mechanism will help uncover targets for therapeutic interventions.

中文翻译：

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缺氧诱导因子 (HIF)-2α 重编程肝巨噬细胞以通过产生白细胞介素 6 来预防急性肝损伤

对乙酰氨基酚 (APAP) 过量是导致急性肝功能衰竭的最常见原因，导致美国超过三分之一的患者死亡或肝移植。唯一的解毒剂 N-乙酰半胱氨酸的有效性在摄入 APAP 后迅速下降，早在患者出现严重肝损伤症状之前就诊。APAP 的直接肝毒性会引发一系列先天免疫反应，这可能会加剧或限制组织损伤的进展。更好地了解这种复杂的机制将有助于发现治疗干预的目标。