Oxidized low-density lipoprotein (ox-LDL) accumulation in the vascular wall plays a pivotal role in the development of atherosclerosis and vascular calcification. However, few studies focus on the regulatory roles of microRNAs in ox-LDL stimulated vascular calcification. The aim of the present study was to investigate how miR-33a-5p regulated vascular calcification stimulated by ox-LDL. In the present study, miR-33a-5p was downregulated during vascular smooth muscle cells (VSMCs) calcification and upon ox-LDL treatment. ox-LDL significantly stimulated VSMCs calcification, while miR-33a-5p overexpression by its mimics transfection inhibited alkaline phosphatase (ALP) activity, mineralization and marker genes associated with VSMCs calcification even in the presence of ox-LDL. Methyltransferase like 3 (METTL3) was the target gene of miR-33a-5p. METTL3 was upregulated during VSMCs calcification and upon ox-LDL treatment. When VSMCs were transfected with miR-33a-5p mimics, METTL3 was downregulated. METTL3 downregulation by siRNA method decreased VSMCs calcification even in the presence of ox-LDL. Taken together, these results suggest miR-33a-5p suppresses VSMCs calcification stimulated by ox-LDL via targeting METTL3, highlighting the critical role of miR-33a-5p/METTL3 in vascular calcification.

血管壁中氧化的低密度脂蛋白 (ox-LDL) 积累在动脉粥样硬化和血管钙化的发展中起关键作用。然而，很少有研究关注 microRNA 在 ox-LDL 刺激的血管钙化中的调节作用。本研究的目的是研究 miR-33a-5p 如何调节 ox-LDL 刺激的血管钙化。在本研究中，miR-33a-5p 在血管平滑肌细胞 (VSMC) 钙化和 ox-LDL 治疗期间下调。ox-LDL显着刺激VSMCs钙化，而miR-33a-5p通过其模拟转染抑制碱性磷酸酶（ALP）活性、矿化和与VSMCs钙化相关的标记基因，即使在ox-LDL存在下也是如此。甲基转移酶样3（METTL3）是miR-33a-5p的靶基因。在 VSMC 钙化和 ox-LDL 治疗期间，METTL3 上调。当用 miR-33a-5p 模拟物转染 VSMC 时，METTL3 被下调。即使在 ox-LDL 存在的情况下，通过 siRNA 方法下调 METTL3 也可降低 VSMC 钙化。总之，这些结果表明 miR-33a-5p 通过靶向 METTL3 抑制 ox-LDL 刺激的 VSMC 钙化，突出了 miR-33a-5p/METTL3 在血管钙化中的关键作用。