在渐进的多发性硬化症中,FABP7的增加,并通过糖溶性开关在单细胞中诱导一种亲炎性表型
Rohit Patel1,2, Devin King1,2, Brenna LaBarre1,2
1Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA.
Nature communications
|July 2, 2025
概括
脂肪酸结合蛋白7 (FABP7) 在渐进的多发性硬化症 (MS) 中升高,导致单细胞炎症并与疾病严重程度相关. FABP7可能是MS的治疗点.
科学领域:
- 神经免疫学 神经免疫学
- 免疫细胞中的代谢途径
- 发现神经退行性疾病的生物标志物.
背景情况:
- 多发性硬化症 (MS) 的特征是先天免疫细胞失调,特别是单细胞,在渐进的阶段.
- 脂肪酸结合蛋白 (FABP) 对于细胞脂肪酸代谢至关重要.
- FABP7,一种特定于大脑的FABP在单细胞功能和MS病变发生中的作用尚未被探索.
研究的目的:
- 在渐进的多发性硬化症的背景下,研究FABP7在单细胞中的作用.
- 为了确定FABP7水平是否与MS残疾和神经病理相关.
- 阐明FABP7影响单细胞功能的分子机制.
主要方法:
- 在二次进展性多发性硬化症患者的血清和脑脊液 (CSF) 中量化FABP7.
- 在死后多发性硬化症脑病变中分析FABP7表达.
- 在体外研究评估FABP7对单细胞基因表达,糖解和炎症标记物的影响.
主要成果:
- 在二次进展性多发性硬化症患者的血清和脑脊液中检测到高FABP7水平.
- 血清FABP7与残疾分数,脑损伤体积和脑体积相对正相关,并且与脑体积相反.
- 在FABP7治疗单细胞的实验室上调CD16,CD80和IL-1β表达,表明增强的炎症,化疗和葡萄糖代谢.
结论:
- 在单细胞中,FABP7促进了促炎特征,这表明它在多发性硬化症的发病过程中发挥了作用.
- FABP7水平与进展性MS中的临床残疾和神经病理标志物相关.
- FABP7是疾病进展的潜在生物标志物,也是渐进性多发性硬化症的治疗点.
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