The histone phosphorylation-related signatures predict prognosis and indicate immune microenvironment infiltration in myocardial infarction

Myocardial infarction (MI) contributes to high global morbidity and mortality rates. Epigenetic regulation plays a key role in MI. The role of histone phosphorylation in MI remains unknown. This study investigated the role of histone phosphorylation-related genes in MI by bioinformatics analysis. The samples of Gene Expression Omnibus (GEO) database were all from humans and the tissue source was blood. We used the GEO database and GeneCards database to obtain histone phosphorylation-related differentially expressed genes (HPRDEGs) associated with MI. We analyzed the Least Absolute Shrinkage and Selection (LASSO) model, Logistic regression model and Support Vector Machine (SVM) model to determine the diagnostic value of 12 HPRDEGs (FASLG, YWHAQ, RPS6, ATM, YWHAZ, KNG1, PRKACA, RPS6KA1, GRB2, MAPK14, PRKCD, RTN3) for MI. A total of 5 Key Genes (FASLG, YWHAZ, KNG1, PRKCD, RTN3) were identified that had high diagnostic value for MI, especially FASLG. According to regulatory network analysis, YWHAZ may be a critical link in the regulatory network associated with histone phosphorylation in MI. FOXA1, E2F1, EGR1, TBP may be the Key TFs that regulate histone-related phosphorylation in MI. The Single-Sample Gene-Set Enrichment Analysis (ssGSEA) algorithm was calculated 28 kinds of immune cell infiltrations in MI. The infiltration abundance of activated CD8 T cells, effector T cells, CD8 memory T follicular helper cells, activated dendritic cells, CD56dim natural killer cells, macrophages, mast cells and neutrophils in High-risk group and Low-risk group of MI was statistically significant. RTN3 was strongly and positively correlated with macrophages and neutrophils. The expression of 5 Key Genes influenced the enrichment of immune cells in MI. This study may provide new insights for regulating histone phosphorylation-related genes as therapeutic targets for MI.