共被期刊论文引用了4次
您的检索式：您选中1篇文献正在查看引证文献汇总
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | 帕金森病基础研究进展显示文摘帕金森病(Parkinson’s disease,PD)是一种常见的中枢神经系统退行性疾病,临床上主要以运动障碍为特征,病理上主要表现为中脑黑质多巴胺能神经元的慢性死亡。目前对PD发病机制的认识尚未完全清楚。近年来,国内外PD的基础研究取得了许多重要进展。本文将从以下五个方面对其中一些进展作简要介绍,即大脑α-突触核蛋白的异常聚集、肠脑轴与PD、多巴胺能神经元死亡的分子机制、线粒体功能障碍和氧化应激、胶质细胞和外周免疫细胞在PD发病过程中的作用等。这些新的进展表明,PD是一种全身性疾病,不仅累及大脑的多巴胺能神经元、胶质细胞,还涉及外周免疫细胞和其他组织器官。这些新的认识对未来发展更精准的诊断和治疗方法具有重要意义。 | 尹舒 周嘉伟 | 2019 | 重庆医科大学学报2019，44，4： | 9 |
| 2 | 星形胶质细胞功能紊乱与中枢神经系统疾病显示文摘星形胶质细胞是中枢神经系统分布最广泛的一类细胞,不仅参与形成三重突触结构和神经血管单元,与其他类型细胞也有紧密复杂的联系。任何形式及不同程度的中枢神经系统损伤和病变,如感染、颅脑损伤、中风、神经退行性疾病等,均会导致星形胶质细胞活化,这种活化伴随特征性结构和功能的变化。随着研究深入,大量证据显示,星形胶质细胞功能降低或失常可能参与了中枢神经系统疾病的发生发展。本文就星形胶质细胞在中风、癫痫、阿尔茨海默症和帕金森综合征发病机制中的保护与损害作用作一综述,旨在为中枢神经系统疾病治疗提供新的思路。 | 闵芳沅 李鑫 王珊 | 2017 | 中南药学2017，15，4： | 7 |
| 3 | Rab蛋白家族在神经类疾病中的作用显示文摘细胞内膜囊泡运输是一个复杂的通路网络,Rab GTPases是膜囊泡运输的主要调节剂,通常被认为是细胞内吞和分泌系统中各种细胞器和囊泡的特异性标记和识别物。与Rab蛋白相关的轴突运输、内体运输发生障碍是造成神经退行性疾病的重要原因之一。本文主要介绍了Rab蛋白在多种神经退行性疾病病理机制中的作用机理与调控机制,同时讨论了线粒体和胶质细胞功能异常与Rab蛋白之间的关联。深入探究Rab蛋白的作用机制对人类神经性疾病的早期诊断和治疗具有潜在的指导意义。 | 吴安平 庆宏 全贞贞 | 2021 | 遗传2021，43，1： | 3 |
| 4 | Suppression of astrocytic autophagy by αB-crystallin contributes to α-synuclein inclusion formation显示文摘Background:Parkinson’s disease(PD)is characterized by a chronic loss of dopaminergic neurons and the presence of proteinaceous inclusions(Lewy bodies)within some remaining neurons in the substantia nigra.Recently,astroglial inclusion body has also been found in some neurodegenerative diseases including PD.However,the underlying molecular mechanisms of how astroglial protein aggregation forms remain largely unknown.Here,we investigated the contribution ofαB-crystallin(CRYAB),a small heat shock protein,inα-synuclein inclusion formation in astrocytes.Methods:Small interfering RNA(siRNA)-mediated CRYAB(siCRYAB)knockdown or CRYAB overexpression was performed to investigate the impact of CRYAB on the autophagy in human glioblastoma cell line U251 cells.Coimmunoprecipitation(co-IP)and immunoblotting were used to dissect the interaction among multiple proteins.The clearance ofα-synuclein in vitro was evaluated by immunocytochemistry.CRYAB transgenic mice and transgenic mice overexpressing A30P mutant form of humanα-synuclein were used to examine the influence of CRYAB toα-synuclein accumulation in vivo.Results:We found that knockdown of CRYAB in U251 cells or primary cultured astrocytes resulted in a marked augmentation of autophagy activity.In contrast,exogenous CRYAB disrupted the assembly of the BAG3-HSPB8-HSC70 complex via binding with BAG3,thereby suppressing the autophagy activity.Furthermore,CRYAB-regulated autophagy has relevance to PD pathogenesis.Knockdown of CRYAB remarkably promoted cytoplasmic clearance ofα-synuclein preformed fibrils(PFFs).Conversely,selective overexpression of CRYAB in astrocytes markedly suppressed autophagy leading to the accumulation of α-synuclein aggregates in the brain of transgenic mice expressing humanα-synuclein A30P mutant.Conclusions:This study reveals a novel function for CRYAB as a natural inhibitor of astrocytic autophagy and shows that knockdown of CYRAB may provide a therapeutic target against proteinopathies such as synucleinopathies. | Shen-zhao Lu Yong-shun Guo Pei-zhou Liang Shu-zhen Zhang Shu Yin Yan-qing Yin Xiao-min Wang Fei Ding Xiao-song Gu Jia-wei Zhou | 2019 | Translational Neurodegeneration2019，8，1： | 2 |
您所在的机构暂未开通此部分的功能，请联系管理员