Targeting Autophagy for Acetaminophen-Induced Liver Injury: An Update

被引：1

作者：

Hinz, Kaitlyn ^{[1
]}

Niu, Mengwei ^{[1
]}

Ni, Hong-Min ^{[1
]}

Ding, Wen-Xing ^{[1
,2
]}

机构：

[1] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol &Therapeut, Kansas City, KS 66160 USA

[2] Univ Kansas, Med Ctr, Dept Internal Med, Kansas City, KS 66160 USA

来源：

LIVERS | 2024年 / 4卷 / 03期

关键词：

mitophagy; NRF2; p62/SQSTM1; TFEB; TRANSCRIPTION FACTOR NRF2; PERSISTENT ACTIVATION; KEAP1-NRF2; PATHWAY; FEEDBACK LOOP; P62; TFEB; HEPATOTOXICITY; P62/SQSTM1; MECHANISM; PROTECTS;

D O I：

10.3390/livers4030027

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

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.

引用

页码：377 / 387

页数：11

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