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在糖尿病足中,USP28通过双化SIRT1蛋白参与高葡萄糖介导的内皮功能障碍

Qiong Liu¹, Jin Zhang², Jichang Bai¹

¹Department of Endocrinology, The Second Hospital of Shijiazhuang, Shijiazhuang, China.

Journal of orthopaedic surgery and research

|September 24, 2025

概括

乌比基特异性酶28 (USP28) 通过稳定静音信息调节器Sirtuin 1 (SIRT1) 来防止高葡萄糖诱导的内皮功能障碍. 针对USP28提供了一种有前途的策略,以改善糖尿病伤口愈合.

科学领域:

内分泌学和新陈代谢学
细胞生物学细胞生物学
伤口治愈研究研究伤口治愈研究

背景情况:

沉默信息调节器Sirtuin 1 (SIRT1) 对于糖尿病伤口愈合至关重要,但易受通过无处不在的降解的破坏.
了解SIRT1二化机制是缓解内皮细胞高葡萄糖诱导损伤的关键.

研究的目的:

调查SIRT1二基化在减轻高葡萄糖 (HG) 诱导的人类静脉内皮细胞 (HUVECs) 损伤中的作用.
阐明在高血糖条件下影响SIRT1稳定性和功能的全素特异性化酶28 (USP28) 的机制.

主要方法:

HUVEC暴露在高葡萄糖 (HG) 中,以模拟高血糖症.
细胞测试评估了生命力,增殖,亡,入侵和血管生成.
评估了铁亡和内细胞网膜应激 (ERS);通过共免疫沉和无处不在测试证实了蛋白质相互作用.

主要成果:

在糖尿病足 (DFU) 患者中观察到较低的血清SIRT1mRNA水平.
USP28对SIRT1进行二氧化和稳定,从而减轻HG诱导的损伤,ERS和HUVEC中的铁亡.
USP28通过稳定SIRT1激活NRF2/HO-1通路,从而提供对HG诱导的内皮功能障碍的保护.

结论:

USP28通过稳定SIRT1和激活NRF2/HO-1通路来缓解高葡萄糖介导的内皮功能障碍.
针对USP28代表了增强糖尿病伤口愈合的潜在治疗途径.

关键词:

糖尿病患者糖尿病患者铁化是铁化的一种.一个SIRT1系统.美国28美元.伤口愈合伤口愈合

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