SARM1 promotes the neuroinflammation and demyelination through IGFBP2/NF‐κB pathway in experimental autoimmune encephalomyelitis mice
SARM1 promotes the neuroinflammation and demyelination through IGFBP2/NF‐κB pathway in experimental autoimmune encephalomyelitis mice
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DOI：
10.1111/apha.13974
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发表时间：
2023-04
影响因子：
6.3
通讯作者：
Jingjing Zhang;Lingting Jin;Xin Hua;Mianxian Wang;Jiaojiao Wang;Xingxing Xu;Huitao Liu;Haoyu Qiu;Hua Sun;T. Dong;Danlu Yang;Xu Zhang;Ying Wang;Zhihui Huang
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文献类型：
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作者：
Jingjing Zhang;Lingting Jin;Xin Hua;Mianxian Wang;Jiaojiao Wang;Xingxing Xu;Huitao Liu;Haoyu Qiu;Hua Sun;T. Dong;Danlu Yang;Xu Zhang;Ying Wang;Zhihui Huang
多发性硬化症（MS）是一种自身免疫性疾病，其典型特征是神经炎症和中枢神经系统（CNS）神经元脱髓鞘。含有1的无菌α和TIR基序（SARM1）是介导轴突变性的重要因子，SARM1缺失可减少脊髓损伤中的神经炎症。本研究旨在探讨SARM1在多发性硬化症中的作用及其潜在机制。
Multiple sclerosis (MS) is an autoimmune disease, and its typical characteristics are neuroinflammation and the demyelination of neurons in the central nervous system (CNS). Sterile alpha and TIR motif containing 1 (SARM1) is an essential factor mediating axonal degeneration and SARM1 deletion reduces the neuroinflammation in spinal cord injury. This study aimed to explore the roles of SARM1 and its underlying mechanisms in MS.