首页|TRAF6与神经退行性疾病关系的研究进展

TRAF6与神经退行性疾病关系的研究进展

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世界人口老龄化趋势愈发明显,神经退行性疾病(neurodegenerative diseases,NDDs)作为一类多发于老年人的常见病备受关注.研究表明,神经炎症是NDDs的一个重要病理特征,肿瘤坏死因子受体相关因子6(tumor necrosis factor receptor-associated factor 6,TRAF6)参与了对神经炎症的调控,并影响NDDs的发生和发展;进一步研究发现TRAF6的这种调控作用与其泛素化作用有关.故本文就TRAF6的分子结构、生物学功能、泛素化机制及其与阿尔茨海默症、帕金森病、多发性硬化症和肌萎缩侧索硬化症这4种常见NDDs的关系加以分析和总结,试图阐明TRAF6调控NDDs发生的可能分子机制,为探讨NDDs病因以及治疗提供一定的理论依据.
Research progress on the relationship between TRAF6 and neurodegenerative diseases
Given the increasing trend of aging population in the world,neurodegenerative diseases(NDDs),a common type of diseases that mostly occur in the elderly,have attracted much more attention.It has been shown that tumor necrosis factor receptor-associated factor 6(TRAF6)is involved in the regulation of neuroinflammation,an important pathological feature of NDDs,and affects the occurrence and development of NDDs.Most importantly,the regulatory effect of TRAF6 is related to its ubiquitination.Therefore,in the present paper,the molecular structure,biological function,and ubiquitination mechanism of TRAF6,and its relationship with some common NDDs,including Alzheimer's disease,Parkinson's disease,multiple sclerosis,and amyotrophic lateral sclerosis,were analyzed and summarized.The possible molecular mechanisms by which TRAF6 regulates the occurrence of NDDs were also elucidated,providing a theoretical basis for exploring the etiology and treatment of NDDs.

tumor necrosis factor receptor-associated factor 6neurodegenerative diseasesneuroinflammationubiquitination

罗瑞昌、吴昕怡、俞雯雯、郑永坚、王丹

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浙江理工大学全省家蚕生物反应器和生物医药重点实验室,杭州 310018

浙江理工大学生命科学与医药学院,杭州 310018

余姚市中医医院药剂科,余姚 315400

肿瘤坏死因子受体相关因子6 神经退行性疾病 神经炎症 泛素化

College Student Science and Technology Innovation Activity Plan(New Talent Plan Project)of Zhejiang Province(2023)Traditional Chinese Medicine Science and Technology Planning Project of Zhejiang ProvinceMedical Science and Technology Project of Ningbo,China

2022ZB3362022Y51

2024

10.13294/j.aps.2024.0041

生理学报
中国科学院上海生命科学研究院,中国生理学会

生理学报

CSTPCD北大核心
影响因子：0.864
ISSN：0371-0874
年,卷(期)：2024.76(4)
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