神经系统中由各种机械和电磁刺激激活的细胞信号通路。

IF 3.5 3区 医学 Q2 NEUROSCIENCES Frontiers in Molecular Neuroscience Pub Date : 2024-10-04 eCollection Date: 2024-01-01 DOI:10.3389/fnmol.2024.1427070
Youngjae Ryu, Aboubacar Wague, Xuhui Liu, Brian T Feeley, Adam R Ferguson, Kazuhito Morioka
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引用次数: 0

摘要

拉伸、剪切应力或压缩等机械刺激可通过细胞的机械传导激活一系列生物分子反应。在神经系统中,对机械应力的研究突出了创伤性损伤和神经退行性疾病的关键病理生理机制。然而,神经系统中机械刺激引发的生物分子途径尚未得到充分探索,尤其是与其他身体系统相比。造成这一知识空白的原因可能是研究中使用的方法和定义多种多样。此外,随着超声波和电磁刺激等机械刺激技术越来越多地用于心理和神经康复治疗,了解其潜在的生物机制对于建立准确的病理生理学模型和加强治疗干预至关重要。本综述旨在总结各种机械和电磁刺激激活的细胞信号通路,尤其关注哺乳动物的神经系统。此外,我们还简要讨论了参与这些过程的潜在细胞机械传感器。
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Cellular signaling pathways in the nervous system activated by various mechanical and electromagnetic stimuli.

Mechanical stimuli, such as stretch, shear stress, or compression, activate a range of biomolecular responses through cellular mechanotransduction. In the nervous system, studies on mechanical stress have highlighted key pathophysiological mechanisms underlying traumatic injury and neurodegenerative diseases. However, the biomolecular pathways triggered by mechanical stimuli in the nervous system has not been fully explored, especially compared to other body systems. This gap in knowledge may be due to the wide variety of methods and definitions used in research. Additionally, as mechanical stimulation techniques such as ultrasound and electromagnetic stimulation are increasingly utilized in psychological and neurorehabilitation treatments, it is vital to understand the underlying biological mechanisms in order to develop accurate pathophysiological models and enhance therapeutic interventions. This review aims to summarize the cellular signaling pathways activated by various mechanical and electromagnetic stimuli with a particular focus on the mammalian nervous system. Furthermore, we briefly discuss potential cellular mechanosensors involved in these processes.

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来源期刊
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.
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