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doi:10.1016/j.molmet.2020.101102

Erastin is capable of triggering ferroptosis in several ways, such as the ability to upregulate SLC7A11 and indirectly downregulate intracellular glutathione levels ( NRF2 can directly or indirectly regulate GPX4 expression and function by increasing the expression of target genes related to iron and ROS metabolism, such as quinone oxidoreductase 1 (NQO1), HO-1 and System Xc- ( ACSL4 is a key enzyme for the synthesis of PUFAs, the raw material for lipid peroxidation, a key component of ferroptosis, and a key target for antiviral activity (e.g., Figure 4B ) ( GPX4 is a peroxide reductase and a key node in the biological function of erastin, and its downregulation can lead to the accumulation of lipid peroxides ( NRF2 , GPX4 and ACSL4 were evaluated for regulation, and erastin treatment of Vero cells exerted its ferroptosis-inducing regulatory role ( In conclusion, erastin activates reactive oxygen species and lipid oxidation in Vero cells, while Fer-1 inhibits this process