对乙酰氨基酚（APAP）是临床上常用的解热镇痛药，过量服用则会造成严重肝损伤甚至死亡。近年来，APAP诱导的肝损伤（AILI）发生率呈上升趋势，已成为全球肝移植的第二大常见原因。自噬是一种高度保守的分解代谢过程，通过溶酶体降解去除不需要的胞质蛋白和细胞器，以实现细胞本身的代谢需要和细胞器的更新。大量研究表明，自噬在AILI的病理生理中起着关键作用，其机制涉及APAP蛋白加合物、氧化应激、JNK活化、线粒体功能障碍、炎症反应和细胞凋亡等。本文通过阐述自噬在AILI中的生物学机制，为AILI的治疗和自噬调节剂的开发提供理论依据。

N-acetyl-p-aminophenol （APAP） is an antipyretic analgesic commonly used in clinical practice， and APAP overdose can cause severe liver injury and even death. In recent years， the incidence rate of APAP-induced liver injury （AILI） tends to increase， and it has become the second most common cause of liver transplantation worldwide. Autophagy is a highly conserved catabolic process that removes unwanted cytosolic proteins and organelles through lysosomal degradation to achieve the metabolic needs of cells themselves and the renewal of organelles. A large number of studies have shown that autophagy plays a key role in the pathophysiology of AILI， involving the mechanisms such as APAP protein conjugates， oxidative stress， JNK activation， mitochondrial dysfunction， inflammatory response and apoptosis. This article elaborates on the biological mechanism of autophagy in AILI， in order to provide a theoretical basis for the treatment of AILI and the development of autophagy regulators.