TFEB
自噬
上睑下垂
溶酶体
多巴胺能
自噬体
帕金森病
细胞生物学
神经科学
疾病
医学
化学
生物
多巴胺
程序性细胞死亡
细胞凋亡
生物化学
病理
酶
作者
Xiaomei Liang,Yaqi Zeng,Piao Zhang,Baoyu Zhu,Jiezhu Feng,Tongtong Deng,Zhongling Fu,Chengshuai Liu,Chengyu Chen,Yuhu Zhang
标识
DOI:10.1186/s12967-025-06634-9
摘要
These findings underscore how PS-NPs accelerated PD onset and progression by disrupting autophagosome-lysosome fusion through TSC2-mTOR-TFEB axis, which triggered protein degradation disorders and pyroptosis in dopaminergic neurons. The molecular mechanisms could inform environmental safety regulations concerning nanoplastics and inspire therapeutic strategies for PD.
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