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内皮Arg2通过影响阿金氨酸代谢来调节HIMM诱导的线粒体过裂

Feng Guo¹, Xinyi Chen², Meijiang Chen²

¹Institute of Traditional Chinese Medicine and Brain Science, Shandong University of Traditional Chinese Medicine, Jinan, China; Institute of Acupuncture and Moxibustion, Shandong University of Traditional Chinese Medicine, Jinan, China.

Free radical biology & medicine

|February 20, 2026

概括

高血糖诱导的代谢记忆 (HIMM) 在内皮细胞中激活阿尔金酶2 (Arg2),导致血管损伤. 阻断Arg2通过恢复阿金氨酸代谢和线粒体功能来防止与HIMM相关的心血管并发症.

科学领域:

心血管生物学心血管生物学
线粒体生物学线粒体生物学
内皮细胞生物学内皮细胞生物学

背景情况:

在糖尿病患者中,尽管控制了葡萄糖,心血管并发症仍然存在.
内皮细胞 (ECs) 中高血糖诱导的代谢记忆 (HIMM) 导致这些并发症,影响线粒体功能.
在HIMM中内皮质阿尔基纳2 (Arg2) 的作用尚不清楚.

研究的目的:

调查内皮质Arg2在HIMM诱导的心血管功能障碍中的作用.
阐明Arg2影响HIMM中阿尔金因代谢和线粒体功能的机制.
评估Arg2作为HIMM相关血管疾病的潜在治疗标.

主要方法:

建立了体内 (HIMM-老鼠模型) 和体内 (HIMM-EC模型) 系统.
利用内皮特异性Arg2过度表达和淘汰的小鼠和细胞系.
评估了Arg2激活,阿尔金因代谢,线粒体功能 (MitoSOX,MitoTracker,OCR) 和血管功能 (超声波,激光光斑,肌谱).

主要成果:

HIMM诱导了Arg2激活,阿金氨酸失调,线粒体功能障碍和血管功能障碍.
内皮层Arg2过度表达模仿HIMM病理,导致内皮层和血管损伤.
内皮Arg2淘汰保护免受HIMM诱导的损伤,恢复氨酸水平,NO-cGMP-PKG信号,并抑制线粒体裂变,改善心血管功能.

结论:

内皮质Arg2在与HIMM相关的血管功能障碍中发挥着关键作用.
二通过氨酸代谢和线粒体裂变来调节血管平衡.
Arg2是高血糖引起的代谢记忆血管疾病的潜在治疗标.

关键词:

阿尔金纳2 2阿尔金纳氨酸的代谢过程由高血糖引起的代谢记忆.脑内皮质功能障碍脑内皮质功能障碍线粒体分裂的线粒体裂变

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