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多发性硬化症中的阿迪波金:免疫失调,神经炎症和治疗机会

Elham Moases Ghaffary¹, Geir Bjørklund², Ramesa Shafi Bhat³

¹Division of Pharmacology and Pharmaceutical Sciences, University of Missouri-Kansas City School of Pharmacy, Kansas City, MO, USA.

Autoimmunity reviews

|May 1, 2025

概括

脂肪组织中的信号分子阿迪波金在多发性硬化症 (MS) 中起着双重作用. 一些通过促进炎症和破坏血脑屏障恶化MS,而另一些则提供神经保护,表明它们作为生物标志物和治疗点的潜力.

科学领域:

神经免疫学神经免疫学
代谢途径代谢途径
中枢神经系统 (CNS) 疾病

背景情况:

多发性硬化症 (MS) 是一种慢性中枢神经系统自身免疫性疾病,其特征是脱髓化和神经炎症.
由脂肪组织分泌的阿迪波金素显著影响免疫和代谢功能.
像抵抗素,瘦素和化学素这样的调节失调的皮素通过促进T细胞炎症和破坏血脑屏障 (BBB) 完整性来加剧MS.

研究的目的:

调查阿迪波金在MS病理生理学和管理中的多方面的作用.
探索阿迪波金作为MS诊断/预后生物标志物的潜力.
评估阿迪波金作为MS的治疗点.

主要方法:

对MS中阿迪波金功能的临床前和翻译研究结果的审查.
在临床MS环境中对阿迪波金表达模式的分析.
考虑生活方式和药物干预措施,以向adipokine配置文件.

主要成果:

阿迪波金在MS中表现出相反的效果:有些是促炎和神经毒性,而阿迪波内克丁表现出免疫调节和神经保护性质.
阿迪波金 (adipokine) 概况与MS预后和诊断相关.
调节阿迪波金水平可能补充现有的疾病修饰治疗 (DMT).

结论:

阿迪波金是MS免疫代谢的关键参与者,影响T细胞,质细胞和BBB功能.
阿迪波金具有作为MS生物标志物和治疗点的巨大潜力.
对阿迪波金介导的免疫代谢调节的进一步研究对于推进MS治疗至关重要.

关键词:

艾迪波基因 (Adipokine) 是一种可怕的药物.生物标志物生物标志物免疫系统的调节失调.多发性硬化症是多发性硬化症.神经炎症是一种神经炎症.治疗目标治疗目标

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