Circular RNAs (circRNAs) have important regulation in thoracic aortic aneurysm (TAA). The function and mechanism of circCDYL (circ_0008285) was explored in TAA here. Angiotensin II (Ang II) was used to construct a TAA model. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed for the detection of circCDYL, miR-1270, and a disintegrin and metalloproteinase 10 (ADAM10). Cell viability was examined via cell counting kit-8 (CCK-8) assay and proliferation was analyzed using Ethynyl-2′-deoxyuridine (EdU) assay. Apoptosis rate was assessed via flow cytometry. Western blot was used for protein detection. Oxidative stress was evaluated by commercial kits. CircCDYL was upregulated in TAA tissues and Ang II-induced circCDYL upregulation in vascular smooth muscle cells (VSMCs). Knockdown of circCDYL weakened Ang II-aroused inhibition of viability, proliferation, and promotion of apoptosis, ferroptosis, and oxidative stress in VSMCs. CircCDYL served as a miR-1270 sponge. The mitigated regulation of circCDYL knockdown for Ang II-induced injury was restored after miR-1270 downregulation. CircCDYL positively regulated ADAM10 through interacting with miR-1270. Overexpression of miR-1270 abated Ang II-induced injury by downregulating ADAM10. In conclusion, circCDYL was involved in the Ang II-induced VSMC injury in TAA via the miR-1270/ADAM10 axis.

中文翻译：

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CircCDYL 有助于 Ang II 诱导的胸主动脉瘤血管平滑肌细胞的凋亡、铁死亡和氧化应激

环状 RNA (circRNA) 在胸主动脉瘤 (TAA) 中具有重要调节作用。circCDYL (circ_0008285) 的功能和机制在 TAA 中进行了探索。使用血管紧张素II（Ang II）构建TAA模型。采用实时定量聚合酶链反应 (RT-qPCR) 检测 circCDYL、miR-1270 以及解整合素和金属蛋白酶 10 (ADAM10)。通过细胞计数试剂盒 8 (CCK-8) 测定检查细胞活力，并使用乙炔基-2'-脱氧尿苷 (EdU) 测定分析增殖。通过流式细胞术评估细胞凋亡率。Western blot用于蛋白质检测。通过商业试剂盒评估氧化应激。CircCDYL 在 TAA 组织中上调，Ang II 诱导血管平滑肌细胞 (VSMC) 中 circCDYL 上调。circCDYL 的敲低减弱了 Ang II 引起的对 VSMC 活力、增殖的抑制，并促进细胞凋亡、铁死亡和氧化应激。CircCDYL 充当 miR-1270 海绵。miR-1270 下调后，circCDYL 敲低对 Ang II 诱导损伤的减弱调节得到恢复。CircCDYL 通过与 miR-1270 相互作用来正向调节 ADAM10。miR-1270 的过表达通过下调 ADAM10 减轻了 Ang II 诱导的损伤。总之，circCDYL 通过 miR-1270/ADAM10 轴参与 Ang II 诱导的 TAA 中 VSMC 损伤。