炎症体
上睑下垂
吡喃结构域
半胱氨酸蛋白酶1
细胞生物学
神经损伤
医学
炎症
神经科学
神经炎症
免疫系统
程序性细胞死亡
免疫学
生物
细胞凋亡
生物化学
作者
Wei Li,Jie Liang,Shaohua Li,Luoyang Wang,Shuo Xu,Suli Jiang,Meiying Song,Haining Meng,Dongchang Zhai,Lei Tang,Yanyan Yang,Li Zhang,Bei Zhang
标识
DOI:10.1016/j.intimp.2022.109026
摘要
Nerve injury and nerve pain are common diseases caused by neuroinflammation. Numerous studies have shown that the activation of NLRP3 (nod-like receptor family, pyrin domain-containing 3) inflammasome is involved in a various inflammatory response, such as Alzheimer's disease, diabetes, nerve damage and other diseases. The NLRP3 inflammasome is a complex containing NLRP3 protein, ASC (apoptosis-associated speckle-like protein), and pro-caspase-1, which is highly expressed and activated to promote the secretion of IL-1β and IL-18 in response to the stimulation of danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) in immune cells such as macrophages and dendritic cells. The activation of NLRP3 inflammasome can cause cell death through caspase-1-mediated cell pyroptosis and plays an important role in the development of nervous system injury and inflammation-related diseases. This discussion aims to summarize the mechanisms of nerve damage and pain caused by excessive activation of the NLRP3 inflammasome.
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