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10.1016/j.cell.2009.03.045 64 KreJ

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In vitro experiments confirmed that A 25-35 treatment significantly inhibited the activation of the NRF2/SLC7A11/GPX4 signaling pathway in HT22 cells, upregulated the expression of Fe 2+ , TFR1, ACSL4, MDA, and GSSG, and decreased the expression of FTH1, SOD, and GSH, as well as the GSH/GSSG ratio, resulting in dysregulated neuronal iron metabolism, impaired amino acid antioxidant systems, mitochondrial dysfunction, and ferroptosis, which ultimately promoted neuronal injury

[PMID: 2272034] PubMed record related to this compound for laboratory literature review

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Excessive ROS damage to vascular endothelial cells disrupts the balance between vasoconstrictive and vasodilatory factors, impairing the hemostatic contractility of spiral arteries