粒体自噬
类有机物
神经科学
MECP2
细胞生物学
神经干细胞
生物
自噬
表型
干细胞
基因
遗传学
细胞凋亡
作者
Jing Zhou,Yuchun Liu,Xintao Jing,Hang Peng,Fang Li,Cao Li,W. Li,Rufeng Li,Jinyuan Zhang,Xiaofei Wang,Jiangfang Lian,Dongdong Tong,Chenfu Huang
标识
DOI:10.1016/j.jare.2025.07.035
摘要
The obtained findings demonstrate that MeCP2 regulates mitophagy by modulating BNIP3L expression, and its dysfunction leads to mitochondrial accumulation and neurodevelopmental abnormalities. The present study highlights the critical role of MeCP2 in maintaining mitochondrial homeostasis and provides insights into the molecular mechanisms underlying MeCP2-related neurodevelopmental disorders.
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