A comprehensive bioinformatics analysis Young-Aged Coronary Heart Disease

Abstract Background Coronary heart disease (CHD) is a leading cause of morbidity and mortality worldwide[1]. Although effective primary and secondary prevention successfully reduced the mortality of CHD, morbidity and mortality of young aged coronary heart disease (YA-CHD) didn’t decrease. However, little is known about the prevalence and mechanism of YA-CHD.Methods Dataset GSE 12288 from Gene Expression Omnibus was imported and performed comprehensive bioinformatics analysis, including gene ontology analysis (GO analysis), pathway analysis, protein-protein interaction network (PPI) analysis and core network analysis.Results RAP1A, which regulates platelet integrin activation and has a critical role in platelet production, was significantly up regulated, while TNKS2, which keeps the integrity of the leukocyte telomere structure and shows a significant association with longevity, was significantly downregulated. Biological process analysis showed “phagosome” pathway was mostly significant related to YA-CHD. Innate immune response module and type I interferon signaling module, interacts with IRF1, may major in the regulation of YA-CHD progression and maybe the potential therapeutic target of YA-CHD.Conclusions RAP1A and TNKS2 in peripheral leukocytes may serve as novel biomarkers in predicting the onset of YA-CHD. Further studies about weather IRF1 influence YA-CHD through regulating innate immune type I interferon signaling pathway was needed.