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Abstract：
With millions of victims worldwide, multiple sclerosis is the second most common cause of disability among young adults. Although formidable advancements have been made in understanding the disease, the neurodegeneration associated with multiple sclerosis is only partially counteracted by current treatments, and effective therapy for progressive multiple sclerosis remains an unmet need. Therefore, new approaches are required to delay demyelination and the resulting disability and to restore neural function by promoting remyelination and neuronal repair.
The article reviews the latest literature in this field.
The fibroblast growth factor (FGF) signaling pathway is a promising target in progressive multiple sclerosis.
FGF signal transduction contributes to establishing the oligodendrocyte lineage, neural stem cell proliferation and differentiation, and myelination of the central nervous system. Furthermore, FGF signaling is implicated in the control of neuroinflammation. In recent years, interventions targeting FGF, and its receptor (FGFR) have been shown to ameliorate autoimmune encephalomyelitis symptoms in multiple sclerosis animal models moderately.
Here, we summarize the recent findings and investigate the role of FGF/FGFR signaling in the onset and progression, discuss the potential therapeutic advances, and offer fresh insights into managing multiple sclerosis.
The article reviews the latest literature in this field.
The fibroblast growth factor (FGF) signaling pathway is a promising target in progressive multiple sclerosis.
FGF signal transduction contributes to establishing the oligodendrocyte lineage, neural stem cell proliferation and differentiation, and myelination of the central nervous system. Furthermore, FGF signaling is implicated in the control of neuroinflammation. In recent years, interventions targeting FGF, and its receptor (FGFR) have been shown to ameliorate autoimmune encephalomyelitis symptoms in multiple sclerosis animal models moderately.
Here, we summarize the recent findings and investigate the role of FGF/FGFR signaling in the onset and progression, discuss the potential therapeutic advances, and offer fresh insights into managing multiple sclerosis.
摘要：
背景：全世界有数百万的受害者，多发性硬化症是年轻人中第二大常见的残疾原因。尽管在了解这种疾病方面取得了令人敬畏的进步，目前的治疗方法只能部分抵消与多发性硬化症相关的神经变性，和进展性多发性硬化症的有效治疗仍未满足需求。因此,需要新的方法来延缓脱髓鞘和由此导致的残疾，并通过促进髓鞘再生和神经元修复来恢复神经功能。
目的：本文综述了该领域的最新文献。
方法：成纤维细胞生长因子（FGF）信号通路是进行性多发性硬化的一个有希望的靶点。
结论：FGF信号转导有助于建立少突胶质细胞谱系，神经干细胞增殖和分化，和中枢神经系统的髓鞘形成。此外，FGF信号传导与神经炎症的控制有关。近年来,针对FGF的干预措施，和其受体（FGFR）已被证明可以适度改善多发性硬化症动物模型中的自身免疫性脑脊髓炎症状。
结论：这里，我们总结了最近的发现，并研究了FGF/FGFR信号在发病和进展中的作用，讨论潜在的治疗进展，并提供管理多发性硬化症的新见解。
目的：本文综述了该领域的最新文献。
方法：成纤维细胞生长因子（FGF）信号通路是进行性多发性硬化的一个有希望的靶点。
结论：FGF信号转导有助于建立少突胶质细胞谱系，神经干细胞增殖和分化，和中枢神经系统的髓鞘形成。此外，FGF信号传导与神经炎症的控制有关。近年来,针对FGF的干预措施，和其受体（FGFR）已被证明可以适度改善多发性硬化症动物模型中的自身免疫性脑脊髓炎症状。
结论：这里，我们总结了最近的发现，并研究了FGF/FGFR信号在发病和进展中的作用，讨论潜在的治疗进展，并提供管理多发性硬化症的新见解。
