自噬
未折叠蛋白反应
细胞生物学
小胶质细胞
内质网
信号转导
神经炎症
化学
生物
细胞凋亡
炎症
免疫学
生物化学
作者
Yuqing Yang,Liang Gao,Jia Meng,Hong Li,Xiaobai Wang,Ying Huang,Jie Wu,Honglin Ma,Dong‐Ying Yan
标识
DOI:10.1016/j.biopha.2023.116053
摘要
Endoplasmic reticulum (ER) stress-induced nerve cell damage has been known to be a hallmark feature of Mn-induced parkinsonism pathogenesis. However, several compensatory machineries, such as unfolded protein response (UPR), autophagy, and immune response, play an essential role in this damage, and the underlying molecular mechanisms are poorly understood.
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