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
免疫学
生物
作者
Wei Li,Jie Liang,Shaohua Li,Luoyang Wang,Shuo Xu,Suli Jiang,Minju 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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