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高血糖调节mTOR信号传递和神经蛋白表达在施万细胞

Nurul Husna Abd Razak¹, Ubashini Vijakumaran¹, Izyan Mohd Idris²

¹Institute of Medical Science Technology, Universiti Kuala Lumpur (UniKL), A1-1, Jalan TKS 1, Taman Kajang Sentral, Kajang 43000, Selangor, Malaysia.

International journal of molecular sciences

|October 16, 2025

概括

高血糖水平会损害在糖尿病外围神经病变 (DPN) 中的施万细胞功能和髓蛋白表达. 该研究发现mTOR信号通路的失调有助于这些变化,为DPN发展提供了洞察力.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
内分泌学在内分泌学.

背景情况:

糖尿病外围神经病变 (DPN) 是一种常见的糖尿病并发症.
施万细胞功能障碍,脱髓化和神经再生受损是DPN的特征.
在高血糖症下施瓦恩细胞表型变化的分子机制尚未完全理解.

研究的目的:

为了研究高葡萄糖对施瓦恩细胞表型的影响.
确定mTOR信号通路在高葡萄糖诱导的 Schwann 细胞变化中的作用.

主要方法:

主要的老鼠施万恩细胞在不同的葡萄糖度 (5mM,25mM,50mM) 中进行培养.
免疫光染色和CTCF分析评估了关键的蛋白质标记物 (c-Jun,Krox-20,p75NTR,MBP,mTOR,p-mTOR,AKR1B1).这些蛋白质标记物包括:

主要成果:

高血糖显著降低了髓基本蛋白 (MBP) 的表达 (p = 0.002).
总mTOR和酸化mTOR (Ser2448) 水平发生显著变化 (分别为p = 0.001和p = 0.0179).
研究结果表明,在高血糖的情况下,mTOR激活受损和髓蛋白损失.

结论:

高血糖引起的mTOR失调是施万细胞反应的一个关键特征.
在 Schwann 细胞中受损的髓蛋白表达有助于 DPN 病变发生.
这项研究为DPN发展提供了分子洞察力.

关键词:

施万细胞重编程的重编程糖尿病周围神经病变过高血糖症 (hyperglycemia) 是一种 mTOR 信号传输系统塑性的可塑性塑性

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