内皮核酸结合寡聚化域类受体蛋白3 动脉样硬化中的炎症酶调节
Shuai Guo1, Litao Wang1,2, Kaixiang Cao1
1School of Basic Medical Sciences, State Key Lab of Respiratory Disease, Guangzhou Medical University, 195 Dongfeng W Rd, Yue Xiu Qu, Guang Zhou Shi, Guang Dong Sheng, China, 510180.
Cardiovascular research
|April 16, 2024
概括
葡萄糖溶解通过改变内皮细胞中的NADH/CtBP1/FOXP1通路来推动动脉样硬化中的NLRP3炎症酶激活. 针对这种途径可能会提供新的动脉样硬化治疗方法.
科学领域:
- 血管生物学 血管生物学
- 免疫学 免疫学 免疫学
- 代谢过程中的代谢.
背景情况:
- 内皮细胞 (EC) NLRP3炎症酶激活驱动动动脉硬化中的血管炎症.
- ECs表现出高的糖解率,这表明糖解在炎症酶激活中发挥了作用.
研究的目的:
- 调查糖解是否以及如何调节动脉样硬化中的内皮NLRP3炎症酶激活.
主要方法:
- 在人类和小鼠动脉样硬化内皮中分析了PFKFB3 (糖解调节剂) 和NLRP3的表达.
- 在Apoe-/-小鼠中利用了EC选择性的Pfkfb3哈普洛缺陷.
- 研究了NADH,CtBP1和FOXP1在调节炎症组分中的作用.
主要成果:
- PFKFB3在动脉样硬化内皮上调,与NLRP3水平相关.
- 缺乏PFKFB3可以减少炎症细胞激活和动脉样硬化.
- 糖解驱动的NADH增加了CtBP1的寡合化,抑制了NLRP3,caspase-1和IL-1β的转抑制.
结论:
- 一个依赖于糖解的NADH/CtBP1/FOXP1通路调节了在动脉生成中的内皮NLRP3炎症酶激活.
- 这一途径是使用PFKFB3抑制剂或CtBP1寡合破坏剂治疗动脉样硬化的潜在治疗标.
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