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Abstract：
Myocardial infarction (MI) is the most serious type of cardiovascular disease and the leading cause of cardiac death.Ferroptosis is one of the newly discovered programmed cell death modes in MI, but its mechanism of action in MI has not been clarified.In this study, we analyzed the expression changes of ferroptosis-related genes in MI and explored the potential mechanisms of ferroptosis-related functions in myocardial infarction. Public data sets GSE19339, GSE97320 and GSE141512 were retrieved from the Gene Expression Omnibus (GEO) Datasets public database. After data preprocessing, differentially expressed genes were screened, and differentially expressed ferroptosis-related genes associated with myocardial infarction were obtained. The biological function and signaling pathway enrichment analysis were performed to establish the PPI interaction network specific to heart tissue, and the differential diagnosis significance of differentially expressed ferroptosis-related genes associated with myocardial infarction was analyzed by ROC curve and decision tree model.A total of 317 genes showed significant changes in expression levels in patients with myocardial infarction, including 205 down-regulated genes and 112 up-regulated genes.Gene Ontology (GO) enrichment analysis and functional classification of Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways showed that these genes were mainly involved in signaling pathways or biological functions related to inflammation and apoptosis.Five differentially expressed ferroptosis-related genes (SLC2A3, EPAS1, HMOX1, ATM, FANCD2) were obtained, all of which played key biological functions in cardiac tissue function. SLC2A3, EPAS1, HMOX1, ATM and FANCD2 genes all had good diagnostic value for myocardial infarction (P < 0.05). The increase of SLC2A3, EPAS1 and HMOX1 are risk factors for myocardial infarction, while ATM and FANCD2 are protective factors.Decision tree analysis showed that SLC2A3, HMOX1, ATM, FANCD2 gene had higher net yield in diagnosing myocardial infarction. In summary, the mechanism of ferroptosis is involved in the occurrence and progression of myocardial infarction. In this study, five differentially expressed ferroptosis-related genes associated with myocardial infarction were retrieved, which may be good biomarkers of ferroptosis after MI.These findings also suggest that the differential expression of ferroptosis-related genes associated with myocardial infarction has significant diagnostic significance for myocardial infarction.
摘要：
心肌梗塞（MI）是最严重的心血管疾病，也是导致心脏死亡的主要原因。Ferroptosis是MI中新发现的程序性细胞死亡模式之一，但其在MI中的作用机制尚未阐明。在这项研究中,我们分析了心肌梗死中铁凋亡相关基因的表达变化，并探讨了心肌梗死中铁凋亡相关功能的潜在机制。从基因表达综合(GEO)数据集公共数据库检索公共数据集GSE191939、GSE97320和GSE141512。数据预处理后,筛选差异表达基因，并获得与心肌梗死相关的差异表达的铁凋亡相关基因。进行生物学功能和信号通路富集分析,建立心脏组织特异性PPI相互作用网络,并通过ROC曲线和决策树模型分析与心肌梗死相关的差异表达铁凋亡相关基因的鉴别诊断意义。共有317个基因在心肌梗死患者中表达水平出现显著变化,包括205个下调基因和112个上调基因。对京都基因和基因组百科全书(KEGG)信号通路的基因本体论(GO)富集分析和功能分类表明,这些基因主要参与炎症和凋亡相关的信号通路或生物学功能。五个差异表达的铁凋亡相关基因（SLC2A3，EPAS1，HMOX1，ATM，获得FANCD2），所有这些都在心脏组织功能中起着关键的生物学功能。SLC2A3、EPAS1、HMOX1、ATM和FANCD2基因对心肌梗死均有较好的诊断价值(P<0.05)。SLC2A3、EPAS1和HMOX1的升高是心肌梗死的危险因素，ATM和FANCD2是保护因素。决策树分析表明,SLC2A3、HMOX1、ATM、FANCD2基因在诊断心肌梗死中具有较高的净产量。总之,铁凋亡的机制与心肌梗死的发生和进展有关。在这项研究中,检索到与心肌梗死相关的五个差异表达的铁凋亡相关基因，这可能是心肌梗死后铁死亡的良好生物标志物。这些发现还表明，与心肌梗死相关的铁凋亡相关基因的差异表达对心肌梗死具有重要的诊断意义。
