Research progress on the mechanisms of c-Jun N-terminal kinase signaling pathway in modulating the expression of important inflammatory mediators in acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is a common clinical critical illness with excessive inflammatory response at its core. c-Jun N-terminal kinase (JNK) is one of the most important members of the mitogen-activated protein kinase (MAPK) family, which plays a role in regulating several important functions including cell proliferation, differentiation, apoptosis, autophagy and inflammation. When the JNK signaling pathway is over-activated, it leads to sustained activation of inflammatory responses and overproduction of inflammatory factors, which can cause serious damage to the organism. Therefore, clarifying the signaling pathways through which JNK participates in the inflammatory response is important for controlling the inflammatory process in ARDS and regulating the balance of the body's immune response.