SCD leads to the development and progression of acute myocardial infarction through the AMPK signaling pathway

Abstract

Abstract Background Acute myocardial infarction (AMI) is myocardial necrosis caused by acute coronary ischemia and hypoxia. It can be complicated by arrhythmia, shock, heart failure and other symptoms that can be life-threatening. A multi-regulator driven dysfunction module for AMI was constructed. It is intended to explore the pathogenesis and functional pathways regulation of acute myocardial infarction. Methods Combining differential expression analysis, co-expression analysis, and the functional enrichment analysis, a set of expression disorder modules related to AMI was obtained. Hypergeometric test was performed to calculate the potential regulatory effects of multiple factors on the module, identifying a range of non-coding RNA and transcription factors. Results A total of 4551 differentially expressed genes for AMI and seven co-expression modules were obtained. These modules are primarily involved in the metabolic processes of prostaglandin transport processes, regulating DNA recombination and AMPK signal transduction. Based on this set of functional modules, 3 of 24 transcription factors (TFs) including NFKB1, MECP2 and SIRT1, and 3 of 782 non-coding RNA including miR-519D-3P, TUG1 and miR-93-5p were obtained. These core regulators are thought to be involved in the progression of AMI disease. Through the AMPK signal transduction, the critical gene stearoyl-CoA desaturase (SCD) can lead to the occurrence and development of AMI. Conclusions In this study, a dysfunction module was used to explore the pathogenesis of multifactorial mediated AMI and provided new methods and ideas for subsequent research. It helps researchers to have a deeper understanding of its potential pathogenesis. The conclusion provides a theoretical basis for biologists to design further experiments related to AMI.