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Smooth muscle NF90 deficiency ameliorates diabetic atherosclerotic calcification in male mice via FBXW7-AGER1-AGEs axis

Author

Listed:
  • Fei Xie

    (Qilu Hospital of Shandong University
    Qilu Hospital of Shandong University)

  • Bin Liu

    (Qilu Hospital of Shandong University
    Qilu Hospital of Shandong University)

  • Wen Qiao

    (Qilu Hospital of Shandong University)

  • Jing-zhen He

    (Qilu Hospital of Shandong University)

  • Jie Cheng

    (Qilu Hospital of Shandong University)

  • Zhao-yang Wang

    (Shandong University)

  • Ya-min Hou

    (Qilu Hospital of Shandong University)

  • Xu Zhang

    (Qilu Hospital of Shandong University)

  • Bo-han Xu

    (Qilu Hospital of Shandong University)

  • Yun Zhang

    (Qilu Hospital of Shandong University)

  • Yu-guo Chen

    (Qilu Hospital of Shandong University
    Qilu Hospital of Shandong University)

  • Ming-xiang Zhang

    (Qilu Hospital of Shandong University)

Abstract

Hyperglycemia accelerates calcification of atherosclerotic plaques in diabetic patients, and the accumulation of advanced glycation end products (AGEs) is closely related to the atherosclerotic calcification. Here, we show that hyperglycemia-mediated AGEs markedly increase vascular smooth muscle cells (VSMCs) NF90/110 activation in male diabetic patients with atherosclerotic calcified samples. VSMC-specific NF90/110 knockout in male mice decreases obviously AGEs-induced atherosclerotic calcification, along with the inhibitions of VSMC phenotypic changes to osteoblast-like cells, apoptosis, and matrix vesicle release. Mechanistically, AGEs increase the activity of NF90, which then enhances ubiquitination and degradation of AGE receptor 1 (AGER1) by stabilizing the mRNA of E3 ubiquitin ligase FBXW7, thus causing the accumulation of more AGEs and atherosclerotic calcification. Collectively, our study demonstrates the effects of VSMC NF90 in mediating the metabolic imbalance of AGEs to accelerate diabetic atherosclerotic calcification. Therefore, inhibition of VSMC NF90 may be a potential therapeutic target for diabetic atherosclerotic calcification.

Suggested Citation

  • Fei Xie & Bin Liu & Wen Qiao & Jing-zhen He & Jie Cheng & Zhao-yang Wang & Ya-min Hou & Xu Zhang & Bo-han Xu & Yun Zhang & Yu-guo Chen & Ming-xiang Zhang, 2024. "Smooth muscle NF90 deficiency ameliorates diabetic atherosclerotic calcification in male mice via FBXW7-AGER1-AGEs axis," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-49315-9
    DOI: 10.1038/s41467-024-49315-9
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    1. Ruisheng Song & Wei Peng & Yan Zhang & Fengxiang Lv & Hong-Kun Wu & Jiaojiao Guo & Yongxing Cao & Yanbin Pi & Xin Zhang & Li Jin & Mao Zhang & Peng Jiang & Fenghua Liu & Shaoshuai Meng & Xiuqin Zhang , 2013. "Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders," Nature, Nature, vol. 494(7437), pages 375-379, February.
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