针对对乙酰氨基酚诱发的肝损伤的自噬作用:最新进展。

Livers Pub Date : 2024-09-01 Epub Date: 2024-08-14 DOI:10.3390/livers4030027
Kaitlyn Hinz, Mengwei Niu, Hong-Min Ni, Wen-Xing Ding
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引用次数: 0

摘要

对乙酰氨基酚(APAP)过量会在实验啮齿动物和人体内诱发肝细胞坏死和急性肝功能衰竭。对乙酰氨基酚主要通过肝脏细胞色素 P450 酶进行代谢,生成高活性代谢物 N-乙酰对苯醌亚胺(NAPQI),形成对乙酰氨基酚蛋白加合物(APAP-adducts),损害线粒体,引发坏死。APAP-加合物和受损的线粒体可以通过自噬选择性地清除。越来越多的证据表明,激活自噬可能对 APAP 诱导的肝损伤(AILI)有益。在本小视图中,我们简要总结了自噬的最新进展,特别是 SQSTM1/p62 和 TFEB 在 AILI 中的药理靶向作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting Autophagy for Acetaminophen-Induced Liver Injury: An Update.

Acetaminophen (APAP) overdose can induce hepatocyte necrosis and acute liver failure in experimental rodents and humans. APAP is mainly metabolized via hepatic cytochrome P450 enzymes to generate the highly reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI), which forms acetaminophen protein adducts (APAP-adducts) and damages mitochondria, triggering necrosis. APAP-adducts and damaged mitochondria can be selectively removed by autophagy. Increasing evidence implies that the activation of autophagy may be beneficial for APAP-induced liver injury (AILI). In this minireview, we briefly summarize recent progress on autophagy, in particular, the pharmacological targeting of SQSTM1/p62 and TFEB in AILI.

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