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.
Subject(s)
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 TransductionABSTRACT
Thymic stromal lymphopoietin (TSLP) is a type I interleukin 2 family cytokine composed of four short-chain α-helix bundles and has homology with interleukin-7. TSLP plays an important role in many allergic diseases or autoimmune diseases, such as asthma, atopic dermatitis, eosinophilic esophagitis, and inflammatory bowel disease, and promotes the development of these diseases. At present, there are some reports on TSLP in liver diseases, and some studies showed that it can promote the development and progression of liver diseases, while others showed that it plays a protective role in liver diseases. This article reviews the molecular composition and biological features of TSLP and the role of TSLP in benign liver diseases and liver tumors and elaborates on the research advances in TSLP in liver diseases.