Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation

摘要: Neuroinflammation is involved in the progression or secondary injury of multiple brain conditions, including stroke and neurodegenerative diseases. Alarmins, also known as damage-associated molecular patterns, are released presence neuroinflammation acute phase ischemia. Defensins, cathelicidin, high-mobility group box protein 1, S100 proteins, heat shock nucleic acids, histones, nucleosomes, monosodium urate microcrystals thought to be alarmins. They from damaged dying cells activate innate immune system by interacting with pattern recognition receptors. Being principal sterile inflammation triggering agents, alarmins considered biomarkers therapeutic targets. recognized host prime toward cell death distress. In stroke, act mediators initiating inflammatory response after release cellular components infarct core penumbra. Increased c-Jun N-terminal kinase (JNK) phosphorylation may mechanism stress-induced Putative crosstalk between alarmin-associated pathways JNK signaling seems inherently interwoven. This review outlines role alarmins/JNK-signaling cerebral neurovascular summarizes complex Emerging anti-JNK anti-alarmin drug treatment strategies discussed.