Fig. 2: Characteristics of DMPs and mediated phenotypes of CAD poor prognosis.
From: DNA methylation predicts adverse outcomes of coronary artery disease
a Enrichment of tissue and cell types by referencing to the histone modification peaks, H3K36me3 (a mark for near transcription termination site) and H3K4me1 (a mark for active enhancers). b Enrichment of tissue and cell types by enhancers and transcription start sites, referencing to the 15 chromatin states in RoadMap Epigenomics. Enh: Enhancer, TxWk: Weak transcription. a, b Statistical enrichment analysis was performed using a binomial test against an array-specific background. c Enrichment of Gene Ontology terms among the prognosis genes. The P-value was computed from the Fisher exact test. d Association of the DMPs with inflammation indices, lipids, and heart functions. Scaled methylation beta values were presented. Significant correlations (P < 0.05) were marked by *. Linear regression was used to identify the relationship between DMPs and clinical phenotypes with age, sex, smoking, and percutaneous coronary intervention adjusted. WBC whole plasma cell count, LMR: lymphocyte-monocyte ratio, NLR neutrophil-lymphocyte ratio, PLR platelet-lymphocyte ratio, FIB fibrinogen, SII systemic immune-inflammation index, LDLC low-density lipoprotein cholesterol, HDLC high-density lipoprotein cholesterol, CHOL total cholesterol, TRIG triglycerides, LVEF left ventricular ejection fraction, LVMI left ventricular mass index. Source data were provided as a Source Data file.
