FER overexpression

To conclude, our research demonstrates that an elevated expression of FXN effectively demonstrates a robust neuroprotective effect against oxidative damage induced by L-Glu. Moreover, it mitigates mitochondrial dysfunction and lipid metabolic dysregulation associated with ferroptosis. FXN overexpression holds promise in potential therapeutic strategies for AD by inhibiting ferroptosis in nerve cells and fostering their protection.

Moreover, ferroptosis inhibitor Fer-1 and MEK1 overexpression both reversed the changes on cell proliferation, apoptosis, and ferroptosis induced by β-eudesmol. β-eudesmol inhibited cell proliferation and promoted cell apoptosis and ferroptosis via regulating MAPK pathway in BC.

In summary, the upregulation of Fer in EC cells resulted in the enhancement of cell proliferation, migration, and invasion through the activation of the Ras-MAPK signaling pathway.

Based on these findings, we concluded that ATF3/Slc7a11 mediated ferroptosis is one of the key mechanisms leading to sorafenib-induced cardiotoxicity. Targeting ferroptosis may be a novel therapeutic approach for preventing sorafenib-induced cardiotoxicity in the future.