Targeting NLRP3 Inflammasome in Translational Treatment of Nervous System Diseases: An Update

炎症体 吡喃结构域 神经保护 免疫系统 先天免疫系统 半胱氨酸蛋白酶1 神经科学 模式识别受体 神经炎症 医学 炎症 免疫学 受体 机制(生物学) 生物 内科学 认识论 哲学
作者
Qingying Yu,Tingting Zhao,Molin Liu,Duanlin Cao,Jiaxin Li,Yanling Li,Mengyao Xia,Xiaoyu Wang,Tingting Zheng,Chuanguo Liu,Xiangyu Mu,Ping Sun
出处
期刊:Frontiers in Pharmacology [Frontiers Media]
卷期号:12 被引量:27
标识
DOI:10.3389/fphar.2021.707696
摘要

Neuroinflammatory response is the immune response mechanism of the innate immune system of the central nervous system. Both primary and secondary injury can activate neuroinflammatory response. Among them, the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome plays a key role in the inflammatory response of the central system. Inflammasome is a type of pattern recognition receptor, a cytoplasmic polyprotein complex composed of members of the Nod-like receptor (NLR) family and members of the pyrin and HIN domain (PYHIN) family, which can be affected by a variety of pathogen-related molecular patterns or damage-related molecular patterns are activated. As one of the research hotspots in the field of medical research in recent years, there are increasing researches on immune function abnormalities in the onset of neurological diseases such as depression, AD, ischemic brain injury and cerebral infarction, the NLRP3 inflammasome causes the activated caspase-1 to cleave pre-interleukin-1β and pre-interleukin-18 into mature interleukin-1β and interleukin-18, in turn, a large number of inflammatory factors are produced, which participate in the occurrence and development of the above-mentioned diseases. Targeted inhibition of the activation of inflammasomes can reduce the inflammatory response, promote the survival of nerve cells, and achieve neuroprotective effects. This article reviews NLRP3 inflammasome's role in neurological diseases and related regulatory mechanisms, which providing references for future research in this field.

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