积累的证据表明，异常调节的环状RNA（circRNA）是心血管疾病，包括急性心肌梗死（AMI）的关键因素。然而，circUSP39在AMI发展中的作用和分子机制仍不清楚。候选circRNA从Gene Expression Omnibus（GEO）数据库（GSE160717）中筛选，并使用GEO2R工具进行分析。使用低氧/再氧化（H/R）诱导的AC16细胞研究circUSP39在心肌细胞H/R损伤中的作用。使用定量实时PCR（qRT-PCR）测试H/R诱导的AC16细胞中的RNA水平。使用细胞计数试剂盒-8、酶联免疫吸附测定、流式细胞术和西方印迹（WB）检测测定细胞存活率、氧化应激、炎症因子水平和细胞凋亡。进行RNA免疫沉淀，RNA拉伸和双荧光素酶报告基因分析以验证circRNA泛素特异性蛋白酶39（circUSP39）、miR-362-3p和肿瘤坏死因子受体相关因子3（TRAF3）之间的相互作用。在H/R诱导的AC16细胞中，circUSP39和TRAF3的表达水平上调，而miR-362-3p的表达水平下调。circUSP39沉默显著提高了H/ R诱导的AC16细胞的细胞存活率和超氧化物歧化酶活性，但减少了丙二醛水平、炎症因子（IL-6、TNF-α，IL-1β和MCP-1）的分泌和细胞凋亡。circUSP39通过吸附miR-362-3p来增加TRAF3的表达，加速H/R诱导的AC16细胞损伤。CircUSP39通过miR-362-3p/TRAF3轴促进了H/R诱导的心肌细胞氧化应激、炎症和凋亡，说明它可能是AMI的治疗靶标。

Accumulating evidence suggested that aberrantly regulated circular RNA (circRNA) is a critical contributor to cardiovascular diseases, including acute myocardial infarction (AMI). However, the role and molecular mechanism of circUSP39 in AMI development remain unclear.Candidate circRNAs were screened from the Gene Expression Omnibus (GEO) database (GSE160717) and analyzed using the GEO2R tool. Hypoxia/reoxygenation (H/R) -induced AC16 cells were used to investigate the function of circUSP39 in H/R injury of cardiomyocytes. Quantitative real-time PCR (qRT-PCR) was employed to test RNA levels in H/R-induced AC16 cells. Cell Counting Kit-8, enzyme-linked immunosorbent assay, flow cytometry, and western blot (WB) assay were used to determine cell viability, oxidative stress, inflammatory factor levels, and cell apoptosis. RNA immunoprecipitation, RNA pull-down, and dual-luciferase reporter assay were conducted to validate the interactions between circRNA ubiquitin-specific peptidase 39 (circUSP39), miR-362-3p, and tumor necrosis factor receptor-associated factor 3 (TRAF3).In H/R-induced AC16 cells, the expression levels of circUSP39 and TRAF3 were upregulated whereas miR-362-3p expression was downregulated. CircUSP39 silencing markedly enhanced cell viability and superoxide dismutase activity but mitigated malondialdehyde level, secretion of inflammatory factors (IL-6, TNF-α, IL-1β, and MCP-1), and cell apoptosis in H/R-induced AC16 cells. CircUSP39 expedited H/R-induced AC16 cell injury by sponging miR-362-3p to increase the expression of TRAF3.CircUSP39 could facilitate H/R-induced cardiomyocyte oxidative stress, inflammation, and apoptosis by the miR-362-3p/TRAF3 axis, elucidating that it might be a therapeutic target for AMI.