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Identification of gene expression profiles in myocardial infarction: A systematic review and meta-analysis

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Συγγραφέας
Kontou P., Pavlopoulou A., Braliou G., Bogiatzi S., Dimou N., Bangalore S., Bagos P.
Ημερομηνία
2018
Γλώσσα
en
DOI
10.1186/s12920-018-0427-x
Λέξη-κλειδί
beta arrestin 2
chemokine receptor CXCR2
chemokine receptor CXCR7
granulocyte chemotactic protein 2
nucleoporin
RANTES
biological marker
carrier protein
transcriptome
ADORA3 gene
ARRB2 gene
Article
bioinformatics
cardiovascular risk
CCL5 gene
CXCL6 gene
CXCR2 gene
CXCR7 gene
disease marker
gene
gene expression profiling
gene identification
gene product
genetic association study
heart infarction
human
incidence
inflammation
NUP37 gene
NUP43 gene
priority journal
quality control
RAE1 gene
RNA processing
RNA transport
systematic review
wound healing
factual database
gene regulatory network
genetics
heart infarction
lipid metabolism
meta analysis
metabolism
signal transduction
Biomarkers
Databases, Factual
Gene Regulatory Networks
Humans
Lipid Metabolism
Membrane Transport Proteins
Myocardial Infarction
Signal Transduction
Transcriptome
BioMed Central Ltd.
Εμφάνιση Μεταδεδομένων
Επιτομή
Background: Myocardial infarction (MI) is a multifactorial disease with complex pathogenesis, mainly the result of the interplay of genetic and environmental risk factors. The regulation of thrombosis, inflammation and cholesterol and lipid metabolism are the main factors that have been proposed thus far to be involved in the pathogenesis of MI. Traditional risk-estimation tools depend largely on conventional risk factors but there is a need for identification of novel biochemical and genetic markers. The aim of the study is to identify differentially expressed genes that are consistently associated with the incidence myocardial infarction (MI), which could be potentially incorporated into the traditional cardiovascular diseases risk factors models. Methods: The biomedical literature and gene expression databases, PubMed and GEO, respectively, were searched following the PRISMA guidelines. The key inclusion criteria were gene expression data derived from case-control studies on MI patients from blood samples. Gene expression datasets regarding the effect of medicinal drugs on MI were excluded. The t-test was applied to gene expression data from case-control studies in MI patients. Results: A total of 162 articles and 174 gene expression datasets were retrieved. Of those a total of 4 gene expression datasets met the inclusion criteria, which contained data on 31,180 loci in 93 MI patients and 89 healthy individuals. Collectively, 626 differentially expressed genes were detected in MI patients as compared to non-affected individuals at an FDR q-value = 0.01. Of those, 88 genes/gene products were interconnected in an interaction network. Totally, 15 genes were identified as hubs of the network. Conclusions: Functional enrichment analyses revealed that the DEGs and that they are mainly involved in inflammatory/wound healing, RNA processing/transport mechanisms and a yet not fully characterized pathway implicated in RNA transport and nuclear pore proteins. The overlap between the DEGs identified in this study and the genes identified through genetic-association studies is minimal. These data could be useful in future studies on the molecular mechanisms of MI as well as diagnostic and prognostic markers. © 2018 The Author(s).
URI
http://hdl.handle.net/11615/75101
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