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.