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. 2017 Mar 16;10:71. doi: 10.3389/fnmol.2017.00071

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Copyright © 2017 Xu, Jiang and Xie.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor 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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Possible interaction between N-methyl-D-aspartate receptors (NMDARs) activation and iron overload. NMDARs activation might promote divalent metal transporter 1 (DMT1)-mediated iron influx via protein kinase A (PKA)-Rhes-DMT1, NO-Dexras1-peripheral benzodiazepine receptor-associated protein 7 (PAP7)-DMT1 signaling cascade pathway and enhance iron releasing from lysosome, then aggravated iron-induced cell damage. In addition, iron overload might stimulate calcium release from endoplasmic reticulum (ER). This indicated that glutamate-induced neurotoxicity and iron participated to a vicious cycle of neuronal death.