Objective. This study is aimed at exploring the underlying molecular mechanisms of ST-segment elevation myocardial infarction (STEMI) and provides potential clinical prognostic biomarkers for STEMI. Methods. The GSE60993 dataset was downloaded from the GEO database, and the differentially expressed genes (DEGs) between STEMI and control groups were screened. Enrichment analysis of the DEGs was subsequently performed using the DAVID database. A protein–protein interaction network was constructed, and hub genes were identified. The hub genes in patients were then validated by quantitative reverse transcription-PCR. Furthermore, hub gene-miRNA interactions were evaluated using the miRTarBase database. Finally, patient data on classical cardiovascular risk factors were collected, and plasma microRNA-146a (miR-146a) levels were detected. An individualized nomogram was constructed based on multivariate Cox regression analysis. Results. A total of 239 DEGs were identified between the STEMI and control groups. Expression of S100A12 and miR-146a was significantly upregulated in STEMI samples compared with controls. STEMI patients with high levels of miR-146a had a higher risk of major adverse cardiovascular events (MACEs) than those with low levels of miR-146a (log-rank ). Multivariate Cox regression analysis identified five statistically significant variables, including age, hypertension, diabetes mellitus, white blood cells, and miR-146a. A nomogram was constructed to estimate the likelihood of a MACE at one, two, and three years after STEMI. Conclusion. The incidence of MACEs in STEMI patients expressing high levels of miR-146a was significantly greater than in those expressing low levels. MicroRNA-146a can serve as a biomarker for adverse prognosis of STEMI and might function in its pathogenesis by targeting S100A12, which may exert its role via an inflammatory response. In addition, our study presents a valid and practical model to assess the probability of MACEs within three years of STEMI.

中文翻译：

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MicroRNA-146a 作为 ST 段抬高心肌梗死不良预后的生物标志物

客观。本研究旨在探索ST段抬高型心肌梗死（STEMI）的潜在分子机制，并为STEMI提供潜在的临床预后生物标志物。方法. 从GEO数据库下载GSE60993数据集，筛选STEMI组与对照组的差异表达基因（DEGs）。随后使用 DAVID 数据库对 DEG 进行了富集分析。构建了蛋白质-蛋白质相互作用网络，并鉴定了中枢基因。然后通过定量逆转录-PCR验证患者的中枢基因。此外，使用 miRTarBase 数据库评估中枢基因-miRNA 相互作用。最后，收集有关经典心血管危险因素的患者数据，并检测血浆 microRNA-146a (miR-146a) 水平。基于多变量 Cox 回归分析构建个性化列线图。结果. 在 STEMI 组和对照组之间共鉴定出 239 个 DEG。与对照相比，STEMI 样品中 S100A12 和 miR-146a 的表达显着上调。与 miR-146a 水平低的患者相比，具有高水平 miR-146a 的 STEMI 患者发生主要不良心血管事件 (MACE) 的风险更高（对数秩）。多变量 Cox 回归分析确定了五个具有统计学意义的变量，包括年龄、高血压、糖尿病、白细胞和 miR-146a。构建列线图以估计 STEMI 后一年、两年和三年发生 MACE 的可能性。结论。表达高水平 miR-146a 的 STEMI 患者的 MACE 发生率显着高于表达低水平的患者。MicroRNA-146a 可作为 STEMI 不良预后的生物标志物，并可能通过靶向 S100A12 在其发病机制中发挥作用，S100A12 可能通过炎症反应发挥作用。此外，我们的研究提出了一个有效且实用的模型来评估 STEMI 三年内发生 MACE 的概率。