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在人类和动物肥胖症中,PFKFB3将糖溶性代谢与内皮功能障碍联系在一起

Robert K Batori¹, Zsuzsanna Bordan¹, Caleb A Padgett¹

¹Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.

Antioxidants (Basel, Switzerland)

|February 26, 2025

概括

肥胖的新陈代谢变化通过增加PFKFB3损害了内皮功能,这破坏了氧化 (NO) 信号传输并增强了氧化的产生,从而导致2型糖尿病的心血管风险.

科学领域:

血管生物学血管生物学
代谢障碍代谢障碍代谢障碍
心血管研究的心血管研究.

背景情况:

肥胖和2型糖尿病 (T2D) 通过代谢失调增加了心血管风险.
内皮功能障碍和氧化物 (NO) 信号受损是早期的后果.
内皮氧化合成酶 (eNOS) 产生NO,但其功能因NADPH氧化酶 (NOXs) 的超氧化物而受损.

研究的目的:

为了研究改变新陈代谢对超氧化物/NO平衡在肥胖症的影响.
阐明糖解酶PFKFB3在内皮功能障碍中的作用.

主要方法:

在T2D患者和肥胖动物模型的内皮细胞 (ECs) 中比较了eNOS表达和NO生物可用性.
在EC中过度表达的PFKFB3,以评估其对NO生产和eNOS激活的影响.
研究了PFKFB3对NADPH氧化酶 (NOX) 活性的影响.
研究了高葡萄糖和TNFα对ECs的PFKFB3表达的影响.

主要成果:

肥胖和T2D模型显示,ECs中的eNOS表达和NO生物可用性下降.
在肥胖动物的EC中,PFKFB3显著增加.
通过增加eNOS-T495酸化和抑制Akt-S473酸化,PFKFB3过度表达减少了NO的产生,从而抑制了eNOS的激活.
PFKFB3增强了NOX1和NOX5活动.
高葡萄糖和TNFα暴露增加了ECs中的PFKFB3表达.

结论:

在肥胖症中,PFKFB3在调解内皮功能障碍方面发挥着关键作用.
增加的PFKFB3通过改变eNOS信号和增强的NOX活性来破坏NO/超氧化物平衡.
这种代谢-PFKFB3-ROS-NO轴代表了一种新的机制,有助于肥胖和T2D中的内皮功能障碍.

关键词:

在NOX1中,NOX1是在NOX5中,NOX5是指NOX5.PFKFB3B3 是一个很好的选择.这就是ROSOS ROS.在 eNOS eNOS 中使用.氧化氧化的使用方法 2 型糖尿病 2 型糖尿病

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