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. 2021 Sep 9;22(5):770. doi: 10.3892/ol.2021.13031

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Copyright: © Li et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — Mechanisms of radiotherapy-induced ferroptosis. IR upregulates the expression of ACSL4, GPX4, SLC7A11 and directly or indirectly increases ROS production. IR combined with IFN-γ inhibits SLC7A11. DNA double-strand breaks induced by IR are able to activate ATM and then inhibit GPX4. ACSL4 and ROS promote lipid peroxidation and lead to ferroptosis. ACSL4, acyl-CoA synthetase long chain family member 4; GPX4, glutathione peroxidase 4; SLC7A11, solute carrier 7A11; ATM, ataxia-telangiectasia mutated; ROS, reactive oxygen species; IR, ionizing radiation.