Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, Hunter James Kelly Research Institute, The State University of New York, University at Buffalo, Buffalo, New York, United States.
Fleni, Buenos Aires, Argentina.
ASN Neuro. 2020 Jan-Dec;12:1759091420962681. doi: 10.1177/1759091420962681.
Iron is a key nutrient for normal central nervous system (CNS) development and function; thus, iron deficiency as well as iron excess may result in harmful effects in the CNS. Oligodendrocytes and astrocytes are crucial players in brain iron equilibrium. However, the mechanisms of iron uptake, storage, and efflux in oligodendrocytes and astrocytes during CNS development or under pathological situations such as demyelination are not completely understood. In the CNS, iron is directly required for myelin production as a cofactor for enzymes involved in ATP, cholesterol and lipid synthesis, and oligodendrocytes are the cells with the highest iron levels in the brain which is linked to their elevated metabolic needs associated with the process of myelination. Unlike oligodendrocytes, astrocytes do not have a high metabolic requirement for iron. However, these cells are in close contact with blood vessel and have a strong iron transport capacity. In several pathological situations, changes in iron homoeostasis result in altered cellular iron distribution and accumulation and oxidative stress. In inflammatory demyelinating diseases such as multiple sclerosis, reactive astrocytes accumulate iron and upregulate iron efflux and influx molecules, which suggest that they are outfitted to take up and safely recycle iron. In this review, we will discuss the participation of oligodendrocytes and astrocytes in CNS iron homeostasis. Understanding the molecular mechanisms of iron uptake, storage, and efflux in oligodendrocytes and astrocytes is necessary for planning effective strategies for iron management during CNS development as well as for the treatment of demyelinating diseases.
铁是中枢神经系统(CNS)正常发育和功能所必需的关键营养素;因此,缺铁和铁过量都可能对 CNS 造成有害影响。少突胶质细胞和星形胶质细胞是脑内铁平衡的关键参与者。然而,在 CNS 发育过程中或在脱髓鞘等病理情况下,少突胶质细胞和星形胶质细胞中铁的摄取、储存和外排的机制尚不完全清楚。在 CNS 中,铁作为参与 ATP、胆固醇和脂质合成的酶的辅助因子,直接参与髓鞘形成,而少突胶质细胞是大脑中含铁量最高的细胞,这与其与髓鞘形成过程相关的代谢需求升高有关。与少突胶质细胞不同,星形胶质细胞对铁的代谢需求不高。然而,这些细胞与血管密切接触,具有很强的铁转运能力。在几种病理情况下,铁动态平衡的变化导致细胞内铁分布和积累的改变以及氧化应激。在多发性硬化等炎症性脱髓鞘疾病中,反应性星形胶质细胞积累铁并上调铁外排和内流分子,这表明它们具备摄取和安全回收铁的能力。在这篇综述中,我们将讨论少突胶质细胞和星形胶质细胞在 CNS 铁稳态中的参与。理解少突胶质细胞和星形胶质细胞中铁摄取、储存和外排的分子机制,对于规划 CNS 发育过程中铁管理以及脱髓鞘疾病治疗的有效策略是必要的。