Xu Huamin, Jiang Hong, Xie Junxia
Collaborative Innovation Center for Brain Science, Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Medical College of Qingdao UniversityQingdao, China; Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Qingdao UniversityQingdao, China.
Front Mol Neurosci. 2017 Mar 16;10:71. doi: 10.3389/fnmol.2017.00071. eCollection 2017.
Both iron dyshomeostasis and N-methyl-D-aspartate receptors (NMDARs)-mediated neurotoxicity have been shown to have an important role in neurological diseases such as Parkinson's disease (PD) and Alzheimer's disease (AD). Evidence proved that activation of NMDARs could promote iron overload and iron-induced neurotoxicity by enhancing iron importer divalent metal transporter 1 (DMT1)-mediated iron uptake and iron releasing from lysosome. Also, iron overload could regulate NMDARs-mediated synaptic transmission. This indicates that there might be a possible relationship between iron and activation of NMDARs in neurological diseases. Understanding this interaction between iron and activation of NMDARs may provide new therapeutic avenues for a more targeted neurotherapeutic strategy for these diseases. Therefore, in this review article, we will describe the dysfunction of iron metabolism and NMDARs in neurological diseases including PD and AD, and summarize the new insight into the mechanisms underlying the interaction between iron and activation of NMDARs.
铁稳态失衡和N-甲基-D-天冬氨酸受体（NMDARs）介导的神经毒性在帕金森病（PD）和阿尔茨海默病（AD）等神经疾病中均发挥重要作用。有证据表明，NMDARs的激活可通过增强铁转运体二价金属离子转运体1（DMT1）介导的铁摄取以及铁从溶酶体的释放，从而促进铁过载和铁诱导的神经毒性。此外，铁过载可调节NMDARs介导的突触传递。这表明在神经疾病中铁与NMDARs的激活之间可能存在某种联系。了解铁与NMDARs激活之间的这种相互作用，可能为这些疾病更具针对性的神经治疗策略提供新的治疗途径。因此，在这篇综述文章中，我们将描述包括PD和AD在内的神经疾病中铁代谢和NMDARs的功能障碍，并总结关于铁与NMDARs激活之间相互作用机制的新见解。
