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There is an urgent need to explore and validate novel biomarkers relevant to patients with myocardial infarction (MI), which is the leading cause of death in the world. Dysregulated microRNAs (miRNAs) and messenger RNAs (mRNAs) based on two Gene Expression Omnibus microarrays were analyzed using bioinformatics technology and experiments. KEGG and GO enrichment analyses were performed to explore potential mechanisms of myocardial infarction progression. Immune infiltration analysis was used to assess the relationship between the immune microenvironment and myocardial infarction. The DOX-induced myocardial injury model was used to simulate myocardial infarction. qRT-PCR was performed to validate the expression of hub genes. 5 downregulated miRNAs and 14 upregulated mRNAs were identified in total. Functional analysis revealed that some immune-related pathways were significantly enriched. T cells CD8+ were mainly enriched in the normal tissues compared to the myocardial infarction tissues. Meanwhile, the T cells CD4+ memory resting were highly enriched in the myocardial infarction tissues compared to the normal tissues. Experimental validation of miRNAs and mRNAs contributed to the identification of 4 miRNAs and 12 mRNAs that may play a crucial role in the DOX-induced myocardial infarction cell model. Our study successfully identified several genes that may be related to myocardial infarction progression.

Acute myocardial infarction is a life-threatening condition with high mortality and complication rates. Although myocardial reperfusion can preserve ischemic myocardial tissue, it frequently exacerbates tissue injury, a phenomenon known as ischemia-reperfusion injury (IRI). However, the underlying pathological mechanisms of IRI remain to be completely understood. Ferroptosis is a novel type of regulated cell death that is associated with various pathological conditions, including angiocardiopathy. The purpose of this article was to elucidate the possible mechanistic role of ferroptosis in IRI through bioinformatics analysis and experimental validation. Healthy and IRI heart samples were screened for differentially expressed ferroptosis-related genes and functional enrichment analysis was performed to determine the potential crosstalk and pathways involved. A protein-protein interaction network was established for IRI, and 10 hub genes that regulate ferroptosis, including HIF1A, EGFR, HMOX1, and ATF3 were identified. In vitro, an anoxia/reoxygenation (A/R) injury model was established using H9c2 cardiomyoblasts to validate the bioinformatics analysis results, and extensive ferroptosis was detected. A total of 4 key hub genes and 3 key miRNAs were also validated. It was found that IRI was related to the aberrant infiltration of immune cells and the small-molecule drugs that may protect against IRI by preventing ferroptosis were identified. These results provide novel insights into the role of ferroptosis in IRI, which can help identify novel therapeutic targets. [ABSTRACT FROM AUTHOR]