神经炎症
裂谷1
肌萎缩侧索硬化
神经退行性变
小胶质细胞
促炎细胞因子
坏死性下垂
信号转导
蛋白激酶A
肿瘤坏死因子α
医学
激酶
细胞生物学
程序性细胞死亡
神经科学
炎症
免疫学
生物
疾病
遗传学
病理
细胞凋亡
作者
Lauren Mifflin,Jun S. Liu,Connor Dufort,Cynthia C. Hession,Alec J. Walker,Kongyan Niu,Hong Zhu,Nan Liu,Jun S. Liu,Joshua Z. Levin,Beth Stevens,Junying Yuan,Chengyu Zou
标识
DOI:10.1073/pnas.2025102118
摘要
Significance Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease. Inhibition of RIPK1, a kinase which regulates cell death and neuroinflammation, has been efficacious in treating mouse models of ALS. RIPK1 inhibitors have reached phase 2 clinical trials in ALS patients. Here, we explore the impact of RIPK1 inhibition on microglial-mediated neuroinflammation in ALS mouse models. We find that there is a subclass of microglia which produces proinflammatory cytokines in a RIPK1-dependent manner, and that this population is reduced by RIPK1 inhibition. We believe that these inflammatory microglia are a hallmark of ALS which may be clinically relevant in advancing RIPK1 inhibitors as a potential ALS therapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI