Li Zhetao, Wang Kuo, Li Ziliang, Chi Yifan
Heart Center, Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), Qingdao, China.
Department of Preventive Treatment, Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), Qingdao, China.
Sci Prog. 2025 Jul-Sep;108(3):368504251366369. doi: 10.1177/00368504251366369. Epub 2025 Aug 12.
The processes of proliferation and migration in endothelial cells are fundamental to the development of atherosclerosis. Recent studies underscore the critical involvement of long noncoding RNAs (lncRNAs) in atherosclerosis by influencing the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Nonetheless, the precise molecular mechanism of lncRNA matrix metalloproteinase 2 antisense RNA 1 (MMP2-AS1) remains inadequately characterized. To investigate this, we established a HUVEC model subjected to transforming growth factor-β1, oxidized low-density lipoprotein, and hypoxia, which resulted in the upregulation of lncRNA MMP2-AS1 expression. Further experimentation demonstrated that knockdown of MMP2-AS1 effectively mitigates the YB-1-mediated enhancement of HUVEC proliferation and migration. Therefore, the primary aim of this research was to explore the role of the MMP2-AS1/YB-1 signaling pathway in atherosclerosis. The findings indicate that MMP2-AS1 regulates HUVEC proliferation and migration through YB-1 targeting. These results suggest that the MMP2-AS1/YB-1 axis holds potential as a therapeutic target for atherosclerosis treatment.
内皮细胞的增殖和迁移过程是动脉粥样硬化发展的基础。最近的研究强调了长链非编码RNA(lncRNAs)通过影响人脐静脉内皮细胞(HUVECs)的增殖和迁移而在动脉粥样硬化中起关键作用。尽管如此,lncRNA基质金属蛋白酶2反义RNA 1(MMP2-AS1)的确切分子机制仍未得到充分阐明。为了研究这一点,我们建立了一个受转化生长因子-β1、氧化型低密度脂蛋白和缺氧作用的HUVEC模型,这导致lncRNA MMP2-AS1表达上调。进一步的实验表明,敲低MMP2-AS1可有效减轻YB-1介导的HUVEC增殖和迁移增强。因此,本研究的主要目的是探索MMP2-AS1/YB-1信号通路在动脉粥样硬化中的作用。研究结果表明,MMP2-AS1通过靶向YB-1调节HUVEC的增殖和迁移。这些结果表明,MMP2-AS1/YB-1轴有望成为动脉粥样硬化治疗的靶点。