Autophagy: a promising process for the treatment of acetaminophen-induced liver injury

Toxicity from drugs has become an important cause of acute liver failure. Acetaminophen, a commonly used analgesic, can cause severe acute liver injury that can worsen into acute liver failure. Autophagy, a protective cell programme, has been reported to have protective effects in a variety of disea...

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Bibliographic Details
Published in:Archives of toxicology 2020-09, Vol.94 (9), p.2925-2938
Main Authors: Tan, Qiuhua, Liu, Yongjian, Deng, Xiaoyi, Chen, Jiajia, Tsai, Ping-Ju, Chen, Pei-Hsuan, Ye, Manxiang, Guo, Jiao, Su, Zhengquan
Format: Article
Language:English
Subjects:
Acetaminophen
Analgesics
Autophagy
Biomedical and Life Sciences
Biomedicine
Drug overdose
Environmental Health
Failure
Hepatocytes
Immunological diseases
Immunosuppressive agents
Inflammatory diseases
Injuries
Liver
Liver diseases
Necrosis
Neurodegenerative diseases
Occupational Medicine/Industrial Medicine
Phagocytosis
Pharmacology/Toxicology
Protein adducts
Review Article
Toxicity
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Summary:Toxicity from drugs has become an important cause of acute liver failure. Acetaminophen, a commonly used analgesic, can cause severe acute liver injury that can worsen into acute liver failure. Autophagy, a protective cell programme, has been reported to have protective effects in a variety of diseases such as cancer, immune diseases, neurodegenerative diseases, and inflammatory diseases. In this review, we describe how an excess of acetaminophen causes liver injury step by step, from the formation of the initial protein adduct to the final hepatocyte necrosis, as well as the induction of autophagy and its beneficial effects on diseases. Emphasis is placed on the potential effect of autophagy on improving the damage of acetaminophen to hepatocytes. Finally, we are committed to providing insights into the treatment of acute liver failure through the mechanism of acetaminophen induced liver injury, the mechanism of autophagy, and the link between autophagy and liver injury.
ISSN:0340-5761
1432-0738
DOI:10.1007/s00204-020-02780-9