The role of JNK signaling pathway in organ fibrosis

• JNK signal pathway participates in various biological processes in tissue fibrosis, such as inflammation, immune response, oxidative stress et al. • Numerous downstream transcription factors and kinases are impacted by the activated JNKs signaling pathway, such as cell activation, differentiation, survival, apoptosis, and so forth. • Studies have revealed distinct and essential roles of JNK signaling pathway during tissue fibrosis. • This review summarize recent molecular mechanism advances of JNK signaling pathway in organ fibrosis, as well as current small molecular Inhibitors and agonists targeting the JNKs, in order to explore a potential therapeutic strategy to organ fibrosis. Fibrosis is a tissue damage repair response caused by multiple pathogenic factors which could occur in almost every apparatus and leading to the tissue structure damage, physiological abnormality, and even organ failure until death. Up to now, there is still no specific drugs or strategies can effectively block or changeover tissue fibrosis. JNKs, a subset of mitogen-activated protein kinases (MAPK), have been reported that participates in various biological processes, such as genetic expression, DNA damage, and cell activation/proliferation/death pathways. Increasing studies indicated that abnormal regulation of JNK signal pathway has strongly associated with tissue fibrosis. This review designed to sum up the molecular mechanism progresses in the role of JNK signal pathway in organ fibrosis, hoping to provide a novel therapy strategy to tackle tissue fibrosis. Recent evidence shows that JNK signaling pathway could modulates inflammation, immunoreaction, oxidative stress and Multiple cell biological functions in organ fibrosis. Therefore, targeting the JNK pathway may be a useful strategy in cure fibrosis.