血管细胞黏附分子1（VCAM1）介导的帕金森病中多巴胺能神经元功能的调节
VCAM1-mediated regulation of dopaminergic neuron function in Parkinson's disease.
作者信息
Oh Mihee, Lee Sunha, Kim Eunhye, Jang Yewon, Han Baek-Soo
机构信息
Biodefense Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
Biodefense Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141; Department of Functional Genomics, University of Science and Technology (UST), Daejeon 34141, Korea.
出版信息
BMB Rep. 2025 May;58(5):217-223. doi: 10.5483/BMBRep.2025-0029.
Parkinson's disease (PD), the second most common neurodegenerative disorder, is characterized by the degeneration of dopaminergic neurons, striatal dopamine deficiency, and the accumulation of intracellular α-synuclein aggregates. This study employed induced pluripotent stem cell (iPSC) technology to generate dopaminergic neurons from somatic cells of both PD patients and healthy controls. The results demonstrate that patient-derived neurons show elevated expression of vascular cell adhesion molecule 1 (VCAM1), which correlates with altered synaptic plasticity, mitochondrial dysfunction, and impaired Rac1 and FAK2 signaling. These findings suggest that VCAM1 plays a pivotal role in PD pathogenesis, and may serve as a potential therapeutic target. [BMB Reports 2025; 58(5): 217-223].
帕金森病（PD）是第二常见的神经退行性疾病，其特征为多巴胺能神经元变性、纹状体多巴胺缺乏以及细胞内α-突触核蛋白聚集体的积累。本研究采用诱导多能干细胞（iPSC）技术，从帕金森病患者和健康对照的体细胞中生成多巴胺能神经元。结果表明，患者来源的神经元显示血管细胞黏附分子1（VCAM1）表达升高，这与突触可塑性改变、线粒体功能障碍以及Rac1和FAK2信号受损相关。这些发现表明，VCAM1在帕金森病发病机制中起关键作用，并可能作为潜在的治疗靶点。[《BMB报告》2025年；58(5): 217 - 223]
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