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甲素D抑制了血管光滑肌细胞中AGE诱导的表型转化

Xingmin He¹, Songhao Tian², Lixia Bu³

¹Fenyang College of Shanxi Medical University, Fenyang, 032200, Shanxi, China.

Scientific reports

|April 3, 2025

概括

甲素D (CTSD) 保护糖尿病中先进的糖化最终产品 (AGEs) 诱导的血管光滑肌细胞 (VSMC) 变化. 过度表达CTSD抑制了AGE驱动的VSMC扩散,迁移和衰老,提供了一个潜在的治疗目标.

科学领域:

生物化学生化学
分子生物学分子生物学
血管生物学血管生物学

背景情况:

糖尿病血管并发症是一个主要的健康问题.
先进的糖化最终产品 (AGEs) 有助于血管功能障碍.
血管光滑肌细胞 (VSMC) 现型转变在这些并发症中起着关键作用.

研究的目的:

研究Cathepsin D (CTSD) 在AGE诱导的VSMC表型转变中的作用.
探索CTSD影响VSMC行为的分子机制.
评估CTSD作为糖尿病血管并发症的潜在治疗点.

主要方法:

在使用lentiviral载体的VSMC中过度表达CTSD.
使用各种测定方法 (CCK-8,EDU,划痕测定方法,SA-β-Gal) 评估VSMC活力,增殖,迁移,衰老和亡.
转录组和代谢组分析以阐明分子机制.

主要成果:

AGEs治疗抑制了内源性CTSD表达,促进了VSMC的增殖,迁移,衰老和亡.
过度表达CTSD抵消了AGE对VSMCs的有害影响.
转录组和代谢组数据表明,CTSD抑制了VSMC中的糖解路径.

结论:

CTSD对AGE诱导的VSMC表型转变起着关键的保护作用.
CTSD可能成为治疗糖尿病血管并发症的新治疗标.
需要进一步的研究才能充分理解CTSD的分子机制和临床应用.

关键词:

先进的糖化最终产品 (AGEs)卡瑟普辛D (CTSD) 是一种现象型转变的变化转录学和代谢学分析.血管光滑肌细胞 (VSMCs) 是一种

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