Roles of ERK signaling pathway in regulating myelination of the peripheral nervous system.

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2025-06-13 eCollection Date: 2025-01-01 DOI:10.3389/fnmol.2025.1617976

Di Liu, Jingwei Zhou

引用次数: 0

Abstract

Myelination of Schwann cells is a complex biological process that plays a crucial role in peripheral nervous system (PNS) development and repair. Recent studies have indicated that the extracellular signal-related kinase (ERK) signaling pathway participates in both developmental PNS myelination and remyelination. This review focuses on recent evidence identifying the roles of the ERK signaling pathway in regulating Schwann cell differentiation, myelination, and remyelination. In addition, the crosstalk between the ERK signaling pathway and other cellular signaling pathways that control Schwann cell myelination, such as c-Jun and Notch, are discussed. This review provides an overview of recent studies, revealing that dysregulated expression of the ERK signaling pathway participated in the pathogenesis of hereditary and acquired peripheral neuropathies.

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ERK信号通路在调节周围神经系统髓鞘形成中的作用。

雪旺细胞髓鞘形成是一个复杂的生物学过程，在周围神经系统（PNS）发育和修复中起着至关重要的作用。最近的研究表明，细胞外信号相关激酶（ERK）信号通路参与了发育性PNS的髓鞘形成和再髓鞘形成。本文综述了近年来有关ERK信号通路在调节雪旺细胞分化、髓鞘形成和再髓鞘形成中的作用的最新证据。此外，本文还讨论了ERK信号通路与控制雪旺细胞髓鞘形成的其他细胞信号通路（如c-Jun和Notch）之间的串扰。本文综述了近年来的研究，揭示了ERK信号通路的表达失调参与了遗传性和获得性周围神经病变的发病机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.