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在REDD1-NF-κB-miRNAs-eNOS/SIRT1轴中介于肥胖引起的内皮细胞衰老和高血压

Yoon Kyung Choi¹, Dong-Keon Lee², Minsik Park²

¹Department of Bioscience and Biotechnology, Konkuk University, Seoul, Republic of Korea.

Nature communications

|March 13, 2026

概括

代谢压力增加REDD1,通过NF-κB和减少eNOS和SIRT1.1的特定微RNA引起血管功能障碍. 这一途径有助于高血压和肥胖症中的脏问题.

科学领域:

血管生物学血管生物学
代谢综合征是代谢综合征的一种.
分子机制的分子机制

背景情况:

血管功能障碍,包括内皮细胞衰老和高血压,是代谢综合征的特征.
驱动这种功能障碍的精确分子机制尚未完全理解.

研究的目的:

研究调节发育和DNA损伤反应1 (REDD1) 在代谢压力诱导的血管功能障碍中的作用.
阐明涉及REDD1,NF-κB,microRNA的信号通路,以及它们在EC中的下游目标.

主要方法:

使用细胞培养 (人类和小鼠EC) 和动物模型 (肥胖小鼠) 进行基因操作 (Redd1淘汰,EC特定的Redd1淘汰,miR-214-3p淘汰,Redd1突变).
评估了EC衰老,高血压,功能和分子标志物,包括REDD1,NF-κB,miR-155-5p,miR-214-3p,eNOS和SIRT1.
研究了IKKβ抑制的影响.

主要成果:

代谢压力调节REDD1,通过NF-κB激活促进EC衰老和高血压.
REDD1诱导miR-155-5p和miR-214-3p,这些抑制ECs中的ENOS和SIRT1表达.
肥胖小鼠的REDD1和miR-214-3p增加,eNOS和SIRT1减少,导致血管和功能障碍;通过针对REDD1或miR-214-3p的基因干预来改善这些影响.

结论:

确定了一个关键的REDD1-非典型的NF-κB-miRNAs-eNOS/SIRT1信号轴,调解肥胖引起的血管功能障碍.
这一途径代表了代谢综合征相关的高血压和血管并发症的潜在治疗标.

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