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对乙酰氨基酚诱导的肝损伤的自噬靶向治疗：最新进展

Targeting Autophagy for Acetaminophen-Induced Liver Injury: An Update.

作者信息

Hinz Kaitlyn, Niu Mengwei, Ni Hong-Min, Ding Wen-Xing

机构信息

Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.

Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA.

出版信息

Livers. 2024 Sep;4(3):377-387. doi: 10.3390/livers4030027. Epub 2024 Aug 14.

DOI:10.3390/livers4030027
PMID:39301093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11412313/
Abstract

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 -acetyl--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.

摘要

对乙酰氨基酚（APAP）过量服用可在实验啮齿动物和人类中诱发肝细胞坏死和急性肝衰竭。APAP主要通过肝细胞色素P450酶代谢，生成高反应性代谢产物N - 乙酰 - 对苯醌亚胺（NAPQI），其形成对乙酰氨基酚蛋白加合物（APAP - 加合物）并损害线粒体，引发坏死。APAP - 加合物和受损的线粒体可通过自噬被选择性清除。越来越多的证据表明，自噬的激活可能对APAP诱导的肝损伤（AILI）有益。在这篇小型综述中，我们简要总结了自噬方面的最新进展，特别是在AILI中对SQSTM1/p62和转录因子EB（TFEB）的药物靶向作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64af/11412313/28a155c0cdf3/nihms-2020099-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64af/11412313/ac7f006f11d5/nihms-2020099-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64af/11412313/28a155c0cdf3/nihms-2020099-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64af/11412313/ac7f006f11d5/nihms-2020099-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64af/11412313/28a155c0cdf3/nihms-2020099-f0002.jpg

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本文引用的文献

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High-throughput screening of novel TFEB agonists in protecting against acetaminophen-induced liver injury in mice.新型TFEB激动剂对乙酰氨基酚诱导的小鼠肝损伤保护作用的高通量筛选
Acta Pharm Sin B. 2024 Jan;14(1):190-206. doi: 10.1016/j.apsb.2023.10.017. Epub 2023 Oct 29.
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Management of Acetaminophen Poisoning in the US and Canada: A Consensus Statement.中美加美沙酮类药物中毒处理共识。
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SQSTM1/p62 and Hepatic Mallory-Denk Body Formation in Alcohol-Associated Liver Disease.
酒精相关性肝病中 SQSTM1/p62 和肝 Mallory-Denk 小体的形成。
Am J Pathol. 2023 Oct;193(10):1415-1426. doi: 10.1016/j.ajpath.2023.02.015. Epub 2023 Mar 9.
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Narirutin activates TFEB (transcription factor EB) to protect against Acetaminophen-induced liver injury by targeting PPP3/calcineurin.橙皮苷通过靶向 PPP3/calcineurin 激活 TFEB（转录因子 EB）来预防对乙酰氨基酚诱导的肝损伤。
Autophagy. 2023 Aug;19(8):2240-2256. doi: 10.1080/15548627.2023.2179781. Epub 2023 Feb 24.
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Mitophagy and endoplasmic reticulum-phagy accelerated by a p62 ZZ ligand alleviates paracetamol-induced hepatotoxicity.由p62 ZZ配体加速的线粒体自噬和内质网自噬减轻对乙酰氨基酚诱导的肝毒性。
Br J Pharmacol. 2023 May;180(9):1247-1266. doi: 10.1111/bph.16004. Epub 2023 Jan 10.
6
Dual roles of p62/SQSTM1 in the injury and recovery phases of acetaminophen-induced liver injury in mice.p62/SQSTM1在对乙酰氨基酚诱导的小鼠肝损伤的损伤和恢复阶段中的双重作用。
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7
Liver-specific deletion of mechanistic target of rapamycin does not protect against acetaminophen-induced liver injury in mice.肝脏特异性敲除雷帕霉素作用机制靶点并不能保护小鼠免受对乙酰氨基酚诱导的肝损伤。
Liver Res. 2021 Jun;5(2):79-87. doi: 10.1016/j.livres.2021.03.001. Epub 2021 Mar 19.
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