神经胶质2 (NG2)细胞:神经炎症相关神经变性的一个有希望的靶点

Q3 Medicine
Zaw Myo Hein , Che Mohd Nasril Che Mohd Nassir , Muhammad Danial Che Ramli , Ibrahim El-Serafi , Banthit Chetsawang
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引用次数: 0

摘要

神经胶质2 (NG2)细胞或多树突细胞是中枢神经系统(CNS)中的动态胶质细胞,与神经炎症和神经退行性疾病(如帕金森病、阿尔茨海默病和多发性硬化症)有关。这些细胞与神经元、星形胶质细胞和小胶质细胞相互作用,调节炎症反应、突触活性和血脑屏障完整性。虽然NG2细胞具有保护作用,但它们的异常激活可能导致疤痕、炎症和神经元变性。方法本文综述了目前关于NG2细胞的分子和功能特性的文献,重点介绍了NG2细胞在神经炎症和神经变性中的作用。相关研究通过在PubMed、Scopus和谷歌Scholar中搜索,使用诸如“NG2细胞”、“神经炎症”和“神经退行性疾病”等关键词来确定。文章的选择基于NG2细胞生物学的相关性、它们与其他胶质细胞的相互作用以及它们的治疗意义。研究结果分为关键主题,包括NG2细胞活化、炎症信号和潜在的治疗靶点。结论ng2细胞在神经炎症和神经退行性变中起关键作用,具有保护和病理双重作用。了解它们的作用机制有助于确定针对NG2细胞活化的治疗策略,包括抗炎药、表观遗传调节剂、天然化合物和单克隆抗体。未来的研究应探索以NG2细胞为靶点的干预措施,以开发治疗中枢神经系统疾病的新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuron-Glial2 (NG2) cells: A promising target for neuroinflammation-related neurodegeneration

Background

Neuron-glial 2 (NG2) cells, or polydendrocytes, are dynamic glial cells in the central nervous system (CNS) that contribute to neuroinflammation and neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. These cells interact with neurons, astrocytes, and microglia, modulating inflammatory responses, synaptic activity, and blood-brain barrier integrity. While NG2 cells have protective roles, their aberrant activation can contribute to scarring, inflammation, and neuronal degeneration.

Methods

This narrative review synthesizes current literature on the molecular and functional properties of NG2 cells with a focus on their involvement in neuroinflammation and neurodegeneration. Relevant studies were identified through searches in PubMed, Scopus, and Google Scholar, using keywords such as “NG2 cells,” “neuroinflammation,” and “neurodegenerative diseases.” Articles were selected based on relevance to NG2 cell biology, their interactions with other glial cells, and their therapeutic implications. Findings were categorized into key themes, including NG2 cell activation, inflammatory signaling, and potential therapeutic targets.

Conclusion

NG2 cells are key players in neuroinflammation and neurodegeneration, serving both protective and pathological roles. Understanding their mechanisms of action can aid in identifying therapeutic strategies targeting NG2 cell activation, including anti-inflammatory agents, epigenetic modulators, natural compounds, and monoclonal antibodies. Future research should explore NG2 cell-targeted interventions to develop novel treatments for CNS disorders.
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来源期刊
CiteScore
2.90
自引率
0.00%
发文量
71
审稿时长
25 days
期刊介绍: Translational Research in Anatomy is an international peer-reviewed and open access journal that publishes high-quality original papers. Focusing on translational research, the journal aims to disseminate the knowledge that is gained in the basic science of anatomy and to apply it to the diagnosis and treatment of human pathology in order to improve individual patient well-being. Topics published in Translational Research in Anatomy include anatomy in all of its aspects, especially those that have application to other scientific disciplines including the health sciences: • gross anatomy • neuroanatomy • histology • immunohistochemistry • comparative anatomy • embryology • molecular biology • microscopic anatomy • forensics • imaging/radiology • medical education Priority will be given to studies that clearly articulate their relevance to the broader aspects of anatomy and how they can impact patient care.Strengthening the ties between morphological research and medicine will foster collaboration between anatomists and physicians. Therefore, Translational Research in Anatomy will serve as a platform for communication and understanding between the disciplines of anatomy and medicine and will aid in the dissemination of anatomical research. The journal accepts the following article types: 1. Review articles 2. Original research papers 3. New state-of-the-art methods of research in the field of anatomy including imaging, dissection methods, medical devices and quantitation 4. Education papers (teaching technologies/methods in medical education in anatomy) 5. Commentaries 6. Letters to the Editor 7. Selected conference papers 8. Case Reports
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