c-Jun N-terminal kinase signaling pathway in acetaminophen-induced liver injury.
10.3760/cma.j.cn121430-20221205-01060
- Author:
Wenshang CHEN
1
;
Jijin ZHU
;
Shilai LI
Author Information
1. Department of Emergency, Guangxi Medical University First Affiliated Hospital, Nanning 530021, Guangxi Zhuang Autonomous Region, China. Corresponding author: Zhu Jijin, Email: Zhujijin63@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Mice;
Acetaminophen/adverse effects*;
Chemical and Drug Induced Liver Injury;
Chemical and Drug Induced Liver Injury, Chronic/metabolism*;
JNK Mitogen-Activated Protein Kinases/metabolism*;
Liver;
Mice, Inbred C57BL;
Signal Transduction
- From:
Chinese Critical Care Medicine
2023;35(11):1223-1228
- CountryChina
- Language:Chinese
-
Abstract:
Acetaminophen (APAP) is the most common antipyretic, analgesic and anti-inflammatory drug, but its overdose often leads to acute liver injury, even acute liver failure, and death in some severe cases. At present, there is still a lack of specific treatments. The c-Jun N-terminal kinase (JNK) signal pathway is one of the potential therapeutic targets identified in recent years in overdose APAP-induced acute liver injury. This article reviews the JNK signaling pathway of APAP in liver metabolism, the activation of JNK signaling pathway and the amplification of oxidative stress, other pathways or cellular processes related to JNK signaling pathway, and the possible challenges of drugs targeting JNK, so as to provide direction and feasibility analysis for further research and clinical application of JNK signaling pathway targets in APAP hepatotoxicity, and to provide reference for searching for other targets.
