解开联系:塌缩素反应介导蛋白 2 磷酸化在神经退行性变和神经再生中的作用。

IF 3.3 4区 医学 Q2 NEUROSCIENCES
Yuebing Wang, Toshio Ohshima
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引用次数: 0

摘要

以神经系统逐渐受损为特征的神经退行性疾病和由神经元损伤引起的神经病都会导致老年人群的神经功能和生活质量严重受损。由于中枢神经系统(CNS)的自我修复能力有限,因此神经损伤和神经退行性疾病的康复是一项重大挑战。研究神经退行性变和再生的机制对于促进我们对神经损伤和退行性疾病的了解和开发有效疗法至关重要,这将显著改善患者的预后。塌缩素反应介导蛋白 2(CRMP2)首次被确定为轴突生长和引导的关键介导因子,对神经发生和神经再生至关重要。磷酸化是 CRMP2 的主要修饰方式,有助于其参与多种生理过程,包括轴突导向、神经可塑性和细胞骨架动力学。先前对 CRMP2 磷酸化的研究已经阐明了它参与神经退行性疾病和神经损伤的机制。改变 CRMP2 磷酸化的药理和基因干预已显示出影响神经退行性疾病和促进神经再生的潜力。即使已有数十年的研究深入探讨了 CRMP2 磷酸化的复杂性,但针对这一主题的综合性文献综述仍然很少。由于缺乏对研究结果的综合和整合,人们无法全面了解 CRMP2 对神经生物学的影响,从而阻碍了该领域的研究进展,进而阻碍了临床治疗和干预措施的潜在进步。本综述旨在汇编有关 CRMP2 磷酸化在神经退行性疾病模型和损伤模型中的作用的研究,以总结其影响并为临床疗法提供新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unraveling the Nexus: The Role of Collapsin Response Mediator Protein 2 Phosphorylation in Neurodegeneration and Neuroregeneration.

Neurodegenerative disease characterized by the progressive damage of the nervous system, and neuropathies caused by the neuronal injury are both led to substantial impairments in neural function and quality of life among geriatric populations. Recovery from nerve damage and neurodegenerative diseases present a significant challenge, as the central nervous system (CNS) has limited capacity for self-repair. Investigating mechanism of neurodegeneration and regeneration is essential for advancing our understanding and development of effective therapies for nerve damage and degenerative conditions, which can significantly enhance patient outcomes. Collapsin response mediator protein 2 (CRMP2) was first identified as a key mediator of axonal growth and guidance is essential for neurogenesis and neuroregeneration. Phosphorylation as a primary modification approach of CRMP2 facilitates its involvement in numerous physiological processes, including axonal guidance, neuroplasticity, and cytoskeleton dynamics. Prior research on CRMP2 phosphorylation has elucidated its involvement in the mechanisms of neurodegenerative diseases and nerve damage. Pharmacological and genetic interventions that alter CRMP2 phosphorylation have shown the potential to influence neurodegenerative diseases and promote nerve regeneration. Even with decades of research delving into the intricacies of CRMP2 phosphorylation, there remains a scarcity of comprehensive literature reviews addressing this topic. This absence of synthesis and integration of findings hampers the field's progress by preventing a holistic understanding of CRMP2's implications in neurobiology, thereby impeding potential advancements in clinical treatments and interventions. This review intends to compile investigations focused on the role of CRMP2 phosphorylation in both neurodegenerative disease models and injury models to summarizing impacts and offer novel insight for clinical therapies.

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来源期刊
NeuroMolecular Medicine
NeuroMolecular Medicine 医学-神经科学
CiteScore
7.10
自引率
0.00%
发文量
33
审稿时长
>12 weeks
期刊介绍: NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.
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