Abstract
Background Identification of potential molecular targets of acute myocardial infarction is crucial to our comprehensive understanding of the disease mechanism. However, studies of gene coexpression analysis via jointing multiple microarray data of acute myocardial infarction still remain restricted. Methods Microarray data of acute myocardial infarction (GSE48060, GSE66360, GSE97320, and GSE19339) were downloaded from Gene Expression Omnibus database. Three data sets without heterogeneity (GSE48060, GSE66360, and GSE97320) were subjected to differential expression analysis using MetaDE package. Differentially expressed genes having upper 25% variation across samples were imported in weighted gene coexpression network analysis. Functional and pathway enrichment analyses were conducted for genes in the most significant module using DAVID. The predicted microRNAs to regulate target genes in the most significant module were identified using TargetScan. Moreover, subpathway analyses using iSubpathwayMiner package and GenCLiP 2.0 were performed on hub genes with high connective weight in the most significant module. Results A total of 1027 differentially expressed genes and 33 specific modules were screened out between acute myocardial infarction patients and control samples. Ficolin (collagen/fibrinogen domain containing) 1 (FCN1), CD14 molecule (CD14), S100 calcium binding protein A9 (S100A9), and mitochondrial aldehyde dehydrogenase 2 (ALDH2) were identified as critical target molecules; hsa-let-7d, hsa-let-7b, hsa-miR-124-3, and hsa-miR-9-1 were identified as potential regulators of the expression of the key genes in the two biggest modules. Conclusions FCN1, CD14, S100A9, ALDH2, hsa-let-7d, hsa-let-7b, hsa-miR-124-3, and hsa-miR-9-1 were identified as potential candidate regulators in acute myocardial infarction. These findings might provide new comprehension into the underlying molecular mechanism of disease.
Highlights
Acute myocardial infarction (AMI) is characterized by definite evidence of myocardial necrosis in a clinical background of acute myocardial ischemia [1]
AMI has a high risk of death due to congestive heart failure and malignant arrhythmia, many endeavors and monies have been spent on developing new therapies, it remains a major challenge for clinicians to prevent the adverse cardiac events and cure this disease
This study aimed to detect out more candidate genes and miRNAs that were involved in the pathogenesis and progression of AMI, among which some genetic biomarkers might be converted into the promising targets for the diagnosis and treatment of AMI
Summary
Acute myocardial infarction (AMI) is characterized by definite evidence of myocardial necrosis in a clinical background of acute myocardial ischemia [1]. AMI has a high risk of death due to congestive heart failure and malignant arrhythmia, many endeavors and monies have been spent on developing new therapies, it remains a major challenge for clinicians to prevent the adverse cardiac events and cure this disease. Established risk factors, such as hypertension, diabetes, hypercholesterolemia, smoking, and obesity, cannot explain all the risk on morbidity and mortality of AMI, and, substantial numbers of patients have an inexplicit etiology in myocardial damage [3]. FCN , CD , S A , ALDH , hsa-let- d, hsa-let- b, hsamiR- - , and hsa-miR- - were identified as potential candidate regulators in acute myocardial infarction These findings might provide new comprehension into the underlying molecular mechanism of disease
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call