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. 2021 Jul 16;12:708645. doi: 10.3389/fphar.2021.708645

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Copyright © 2021 Wang, Wang, Cao, Dong and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hypothetical diagram of how melatonin improves SD-induced hippocampal ferroptosis. Exogenous melatonin likely alleviates hippocampal ferroptosis caused by acute SD through by binding to the MT2 receptor and activating ERK/Nrf2 signaling, thereby improving lipid peroxidation and iron transporter disorder. ARE, antioxidant response element; CP, ceruloplasmin; DMT1, divalent metal transporter 1; ERK1/2, extracellular regulated protein kinases; FPN, ferroportin; GPX4, glutathione peroxidase 4; Keap1, Kelch-like ECH-associated protein 1; Mel, melatonin; ML385, Nrf2 inhibitor; MDA, malondialdehyde; MT2, melatonin receptor 2; Nrf2, nuclear factor erythroid 2-related factor 2; PD98059, ERK inhibitor; ROS, reactive oxygen species; SD, sleep deprivation; SOD, superoxide dismutase; STEAP3, 6-transmembrane epithelial antigen of the prostate 3; TFR1, transferrin receptor 1; 4P-PDOT, 4-phenyl-2-propionamidotetralin.