scholarly journals Potential role of a three-gene signature in predicting diagnosis in patients with myocardial infarction

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 2734-2749
Author(s):  
Yinhui Yao ◽  
Jingyi Zhao ◽  
Xiaohui Zhou ◽  
Junhui Hu ◽  
Ying Wang
Keyword(s):  
Myocardial Infarction ◽  
Potential Role ◽  
Gene Signature

scholarly journals Potential Role of a Three-Gene Signature for Predicting Diagnosis in Patients With Myocardial Infarction

2021 ◽  
Author(s):  
Yinhui Yao ◽  
Jingyi Zhao ◽  
Xiaohui Zhou ◽  
Ying Wang
Keyword(s):  
Myocardial Infarction ◽  
Logistic Regression ◽  
Roc Curve ◽  
Potential Role ◽  
Meta Analysis ◽  
Gene Signature ◽  
Diagnostic Value ◽  
Functional Enrichment ◽  
Healthy Control

Abstract ObjectiveIncreasing evidence underscored that the expression of genes was associated with the development and progression of myocardial infarction (MI). In this study, We evaluated the diagnostic value of the feature genes in MI based on data from the Gene Expression Omnibus (GEO) database.MethodsWe used the data from the GEO database (GSE66360) to identify a set of significant differentially expressed genes (DEGs) between MI and healthy control. Univariable logistic regression, the least absolute shrinkage and selection operator (LASSO), SignalP 3.0 server and multivariable logistic regression were used to find the potential role of genes for predicting diagnosis in patients with MI. Receiver operating characteristic (ROC) curve analyses, area under the curve (AUC) and C-index were used to estimate the diagnostic value of genes in patients with MI. The validation for the association was conduct in another six independent data sets (GSE141512, GSE24519, GSE34198, GSE48060, GSE60993, and GSE109048). Then, a meta-analysis was performed to evaluate the diagnostic value of genes in MI.ResultsA total of 44 DEGs were selected from GSE66360. Functional enrichment and KEGG analysis were performed to reveal the DEGs in some inflammation-related biological processes and pathways. A three-gene signature consisted of CCL20, IL1R2 and ITLN1, which could effectively distinguish patients in MI (AUC and C-index were the same value of 0.975). The three-gene signature was effectively validated in 7 independent cohorts, and diagnostic meta-analysis results of the three-gene signature showed that the pooled sensitivity, specificity and ROC curve AUC for MI were0.82 (95% CI: 0.68-0.90), 0.91 (95% CI: 0.81-0.96) and 0.94(95%CI, 0.91-0.96), respectively. ConclusionIt was magnificently suggest that the three-gene signature might potentially serve as novel candidate biomarkers for distinguishing MI from healthy control. Besides, more well-designed cohort studies need to be implemented to warrant the diagnostic value of three-gene signature in clinical purpose.

scholarly journals Microarray Expression Profile of Circular RNAs in Heart Tissue of Mice with Myocardial Infarction-Induced Heart Failure

2016 ◽  
Vol 39 (1) ◽  
pp. 205-216 ◽  
Author(s):  
Hong-Jin Wu ◽  
Cheng-Ying Zhang ◽  
Sai Zhang ◽  
Min Chang ◽  
Hong-Yun Wang
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Potential Role ◽  
Expression Patterns ◽  
Heart Tissue ◽  
Circular Rnas ◽  
Global Changes ◽  
Microarray Expression ◽  
Microarray Expression Profile

Background/Aims: Myocardial infarction (MI) is a serious complication of atherosclerosis associated with increasing mortality attributable to heart failure. This study is aimed to assess the global changes in and characteristics of the transcriptome of circular RNAs (circRNAs) in heart tissue during MI induced heart failure (HF). Methods: Using a post-myocardial infarction (MI) model of HF in mice, we applied microarray assay to examine the transcriptome of circRNAs deregulated in the heart during HF. We confirmed the changes in circRNAs by quantitative PCR. Results: We revealed and confirmed a number of circRNAs that were deregulated during HF, which suggests a potential role of circRNAs in HF. Conclusions: The distinct expression patterns of circulatory circRNAs during HF indicate that circRNAs may actively respond to stress and thus serve as biomarkers of HF diagnosis and treatment.

Inhibition of sphingomyelin synthase 2 relieves hypoxia-induced cardiomyocyte injury by reinforcing Nrf2/ARE activation via modulation of GSK-3β

2020 ◽  
pp. 096032712096995
Author(s):  
Aiping Jin ◽  
Haijuan Cheng ◽  
Lina Xia ◽  
Sha Ye ◽  
Cuiling Yang
Keyword(s):  
Myocardial Infarction ◽  
Potential Role ◽  
Glycogen Synthase ◽  
Tissue Injury ◽  
Cardiac Injury ◽  
Ros Generation ◽  
Related Factor ◽  
Loss Of Function ◽  
Sphingomyelin Synthase

Sphingomyelin synthase 2 (SMS2) is a vital contributor to tissue injury and affects various pathological processes. However, whether SMS2 participates in the modulation of cardiac injury in myocardial infarction has not been determined. This study aimed to evaluate the potential role of SMS2 in the regulation of cardiomyocyte injury induced by hypoxia, an in vitro model for studying myocardial infarction. Our data revealed that SMS2 expression was significantly upregulated in cardiomyocytes in response to hypoxia. Loss-of-function experiments revealed that knockdown of SMS2 markedly restored the viability of cardiomyocytes impaired by hypoxia, and attenuated hypoxia-evoked apoptosis and reactive oxygen species (ROS) generation. In contrast, cardiomyocytes that highly expressed SMS2 were more sensitive to hypoxia-induced injury. Moreover, SMS2 deficiency enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling through inactivation of glycogen synthase kinase-3β. Notably, suppression of Nrf2 markedly abrogated SMS2 knockdown-mediated cardioprotective effects on hypoxia-exposed cardiomyocytes. Our results illustrate that downregulation of SMS2 exerts a cardioprotective function by protecting cardiomyocytes from hypoxia-induced apoptosis and oxidative stress through enhancement of Nrf2 activation. Our study indicates a potential role of SMS2 in the modulation of cardiac injury, which may contribute to the progression of myocardial infarction.

scholarly journals IL-37—a putative therapeutic agent in cardiovascular diseases

QJM ◽  
2021 ◽  
Author(s):  
S McCurdy ◽  
J Yap ◽  
J Irei ◽  
J Lozano ◽  
W A Boisvert
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Diseases ◽  
Potential Role ◽  
Therapeutic Agent ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Orphan Receptor ◽  
Elevated Plasma ◽  
Coronary Syndrome

Summary Although it is a member of the Interleukin (IL)-1 family, IL-37 is unique in that it has wide-ranging anti-inflammatory characteristics. It was originally thought to prevent IL-18-mediated inflammation by binding to the IL-18-binding protein. However, upon discovery that it binds to the orphan receptor, IL-1R8, further studies have revealed an expanded role of IL-37 to include several intracellular and extracellular pathways that affect various aspects of inflammation. Its potential role specifically in cardiovascular diseases (CVD) stemmed initially from the discovery of elevated plasma IL-37 levels in human patients with acute coronary syndrome and atrial fibrillation. Other studies using mouse models of ischemia/reperfusion injury, vascular calcification and myocardial infarction have revealed that IL-37 can have a beneficial role in these conditions. This review will explore recent research on the effects of IL-37 on the pathogenesis of CVD.

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