Conclusion
Intentional or unintentional overdose of acetaminophen leads to Acetaminophen-induced liver injury, which is the most common cause of acute liver injury in the United States and most western countries. C-Jun N terminal kinase (JNK) may is a potential target for treatment of APAP-induced liver injury, therefore, this review explored the essential role of JNK signaling pathway in various stages of APAP hepatotoxicity. JNK signaling pathway mediates APAP metabolism, especially GSH metabolism, amplifies mitochondrial oxidative stress, accelerates injury of liver cells, and mediates apoptotic or necrotic and other forms of cells death. In addition, JNK signaling pathway play a key role in endogenous immunity and non-parenchymal cells. Moreover, JNK signaling pathway induces regeneration of liver cells after cell death.