Xu Huamin, Wang Youcui, Song Ning, Wang Jun, Jiang Hong, Xie Junxia
Collaborative Innovation Center for Brain Science, Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Medical College of Qingdao University, Qingdao, China.
Front Mol Neurosci. 2018 Jan 19;10:455. doi: 10.3389/fnmol.2017.00455. eCollection 2017.
It is now increasingly appreciated that glial cells play a critical role in the regulation of iron homeostasis. Impairment of these properties might lead to dysfunction of iron metabolism and neurodegeneration of neurons. We have previously shown that dysfunction of glia could cause iron deposit and enhance iron-induced degeneration of dopamine (DA) neurons in Parkinson's disease (PD). There also has been a substantial growth of knowledge regarding the iron metabolism of glia and their effects on iron accumulation and degeneration of DA neurons in PD in recent years. Here, we attempt to describe the role of iron metabolism of glia and the effect of glia on iron accumulation and degeneration of DA neurons in the substantia nigra of PD. This could provide evidence to reveal the mechanisms underlying nigral iron accumulation of DA neurons in PD and provide the basis for discovering new potential therapeutic targets for PD.
现在人们越来越认识到神经胶质细胞在铁稳态调节中起着关键作用。这些特性的损害可能导致铁代谢功能障碍和神经元神经变性。我们之前已经表明，神经胶质细胞功能障碍可导致铁沉积，并增强帕金森病（PD）中多巴胺（DA）神经元的铁诱导变性。近年来，关于神经胶质细胞的铁代谢及其对PD中DA神经元铁积累和变性的影响的知识也有了大幅增长。在这里，我们试图描述神经胶质细胞铁代谢的作用以及神经胶质细胞对PD黑质中DA神经元铁积累和变性的影响。这可以为揭示PD中DA神经元黑质铁积累的潜在机制提供证据，并为发现PD新的潜在治疗靶点提供基础。
