ArticleEuropean journal of medical research2026
Notch-1 suppressed vascular dementia via modulating AMPK/mTOR/TFEB/YAP signaling induced ferroptosis.
Article in European journal of medical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe aim of this study is to clarify the molecular mechanism by which Notch-1 prevents vascular dementia (VD) by preventing ferroptosis caused by the AMPK/mTOR/TFEB/YAP pathway.
methodsThirty male SD rats were used in the in vivo tests. They were split into three groups at random: the sham group, the model group, and the model + Notch1-OE group. The water maze test was used to evaluate the rats' spatial learning and memory capacities. Western blotting was done to look at protein expression in hippocampus tissues, and Nissl staining was utilized to see changes in Nissl bodies. Purchased hippocampus cells were used in in vitro tests, and they were split up into six groups and exposed to various stimuli. Fe
resultsIn vivo, rats with VD treated with Notch1-OE demonstrated enhanced spatial learning and memory, reduced neuronal damage, elevated Nissl bodies, increased expression of the SLC7A11 protein, and significantly decreased expression of the NCOA4 protein. According to in vitro studies, Notch-1 reduced Fe2 + levels, prevented ferroptosis, and decreased apoptosis of hippocampus cells by suppressing P-AMPK and nuclear TFEB protein expression and increasing p-mTOR and nuclear YAP protein production. This, in turn, prevented the development of VD.
conclusionBy modifying the AMPK/mTOR/TFEB/YAP signaling pathway, Notch-1 inhibits VD and controls ferroptosis.
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