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.

铁是正常中枢神经系统 (CNS) 发育和功能的关键营养素；因此，缺铁和铁过量都可能对中枢神经系统产生有害影响。少突胶质细胞和星形胶质细胞是脑铁平衡的关键参与者。然而，在中枢神经系统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摄取、储存和流出的机制尚不完全清楚。在中枢神经系统中，髓鞘生成直接需要铁，作为参与 ATP、胆固醇和脂质合成的酶的辅助因子，少突胶质细胞是大脑中铁含量最高的细胞，这与其代谢需求升高有关髓鞘形成。与少突胶质细胞不同，星形胶质细胞对铁的代谢需求并不高。然而，这些细胞与血管紧密接触，具有很强的铁转运能力。在几种病理情况下，铁稳态的变化导致细胞铁分布和积累以及氧化应激的改变。在多发性硬化症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流出和流入分子，这表明它们能够吸收和安全地回收铁。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。了解少突胶质细胞和星形胶质细胞中铁摄取、储存和流出的分子机制对于规划中枢神经系统发育过程中铁管理的有效策略以及治疗脱髓鞘疾病是必要的。这些细胞与血管紧密接触，具有很强的铁转运能力。在几种病理情况下，铁稳态的变化导致细胞铁分布和积累以及氧化应激的改变。在多发性硬化症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流出和流入分子，这表明它们能够吸收和安全地回收铁。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。了解少突胶质细胞和星形胶质细胞中铁摄取、储存和流出的分子机制对于规划中枢神经系统发育过程中铁管理的有效策略以及治疗脱髓鞘疾病是必要的。这些细胞与血管紧密接触，具有很强的铁转运能力。在几种病理情况下，铁稳态的变化导致细胞铁分布和积累以及氧化应激的改变。在多发性硬化症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流出和流入分子，这表明它们能够吸收和安全地回收铁。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。了解少突胶质细胞和星形胶质细胞中铁摄取、储存和流出的分子机制对于规划中枢神经系统发育过程中铁管理的有效策略以及治疗脱髓鞘疾病是必要的。