关键词: AKT/mTOR LINGO1 Multiple sclerosis Notch Nrf2 RXR-γ Remyelination Wnt/β Catenin

Mesh : Humans Multiple Sclerosis / drug therapy Remyelination Oligodendroglia / metabolism pathology Neurodegenerative Diseases / metabolism Myelin Sheath / metabolism pathology

来  源:   DOI:10.1007/s00109-023-02312-9

Abstract:
Multiple sclerosis is an autoimmune neurodegenerative disease of the CNS that causes progressive disabilities, owing to CNS axon degeneration as a late result of demyelination. In the search for the prevention of axonal loss, mitigating inflammatory attacks in the CNS and myelin restoration are two possible approaches. As a result, therapies that target diverse signaling pathways involved in neuroprotection and remyelination have the potential to overcome the challenges in the development of multiple sclerosis treatments. LINGO1 (Leucine rich repeat and Immunoglobulin domain containing, Nogo receptor- interaction protein), AKT/PIP3/mTOR, Notch, Wnt, RXR (Retinoid X receptor gamma), and Nrf2 (nuclear factor erythroid 2-related factor 2) signaling pathways are highlighted in this section. This article reviews the present knowledge regarding numerous signaling pathways and their functions in regulating remyelination in multiple sclerosis pathogenesis. These pathways are potential biomarkers and therapeutic targets in MS.
摘要:
多发性硬化症是中枢神经系统的自身免疫性神经退行性疾病,会导致进行性残疾,由于脱髓鞘晚期导致中枢神经系统轴突变性。在寻求预防轴突丢失的过程中,减轻中枢神经系统的炎症发作和髓鞘恢复是两种可能的方法.因此,靶向涉及神经保护和髓鞘再生的不同信号通路的疗法有可能克服多发性硬化症治疗发展中的挑战.LINGO1(富含亮氨酸的重复序列和免疫球蛋白结构域,Nogo受体-相互作用蛋白),AKT/PIP3/mTOR,缺口,Wnt,RXR(视黄醇X受体γ),和Nrf2(核因子红系2相关因子2)信号通路在本节中重点介绍。本文回顾了有关许多信号通路及其在多发性硬化症发病机理中调节髓鞘再生的功能的现有知识。这些途径是MS的潜在生物标志物和治疗靶标。
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