Novel roles of Nrf3–Trim5 axis in vascular smooth muscle cell dysfunctions and neointimal hyperplasia
We comprehensively demonstrate that Nrf3 is a novel modulator in VSMC dysfunctions and injury-induced NIH. Nrf3 exerts its pathological functions by transcriptional activation of Trim5 gene, which in turn triggers autophagy in VSMCs and injured arteries, promoting arterial remodelling. Inhibiting the Nrf3-Trim5 signal axis ameliorates injury-induced NIH, offering novel therapeutics for treating patients with NIH-related vascular diseases.
Authors
- Li Zhang (ORCID: https://orcid.org/0000-0002-0007-198X)
- Leyu Wang (ORCID: https://orcid.org/0000-0002-5961-7764)
- Qingzhong Xiao (ORCID: https://orcid.org/0000-0001-9101-0498)
- Ancheng Zheng (ORCID: https://orcid.org/0000-0003-0929-3703)
- Kun Sun (ORCID: https://orcid.org/0000-0002-0504-7372)
- Yumeng Wang (ORCID: https://orcid.org/0000-0002-7060-3224)
- Zhenning Shi (ORCID: https://orcid.org/0009-0004-9194-7810)
- Shasha Sun
- Xiaolei Xu (ORCID: https://orcid.org/0000-0003-3168-4743)
- Mei Yang (ORCID: https://orcid.org/0000-0002-2208-9339)
- Qishan Chen (ORCID: https://orcid.org/0000-0002-4642-0866)
Institutions
- Queen Mary University of London (GB)
- XinHua Hospital (CN)
- William Harvey Research Institute (GB)
Publication Details
- Journal
- Cardiovascular Research
- Published
- 2025-05-16
- DOI
- https://doi.org/10.1093/cvr/cvaf084
- Citations
- 4
- Primary Topic
- Genomics, phytochemicals, and oxidative stress
- Type
- article
- Field-Weighted Citation Impact
- 3.22
Funders
- Natural Science Foundation of Shanghai
- British Heart Foundation
- National Natural Science Foundation of China
- National Key Research and Development Program of China
- Natural Science Foundation of Zhejiang Province