High Expression Levels of the <i>SOCS3</i> Gene Are Associated with Acute Myocardial Infarction

Meng, Heyu; Wang, Xue; Ruan, Jianjun; Chen, Weiwei; Meng, F.; Yang, Ping

doi:10.1089/gtmb.2020.0040

Cited by 16 publications

(15 citation statements)

References 37 publications

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“…Recently, mRNAs and microRNAs have emerged as promising biomarkers in cardiovascular disease in general and in AMI in particular. For example, SOCS3 could serve as a biomarker to predict the risk of AMI, where the elevated expression of the SOCS3 gene is an independent risk factor for AMI (16). In particular, miR-34, which is known to modulate immunity, was found to be significantly modulated in post-MI heart failure, providing important information on its role in heart failure (29,30).…”

Section: Discussionmentioning

confidence: 99%

“…For example, the expression of FFAR2, also known as GPR43, in AMI patients has been found to be notably lower than in the controls, and low levels of FFAR2 expression in peripheral blood was confirmed as an independent risk predictor for AMI, with an odds ratio of 6.308 (15). The upregulation of the suppressor of cytokine signaling 3 (SOCS3) gene increases the risk of AMI by potentiating inflammatory responses (16). Moreover, research has shown that immune cell infiltration plays an increasingly significant role in the occurrence and development of various diseases (11,(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

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Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction

Zhao

Xie

Zhang

2020

Front. Cardiovasc. Med.

103

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The present study was designed to identify potential diagnostic markers for acute myocardial infarction (AMI) and determine the significance of immune cell infiltration in this pathology. Methods: Two publicly available gene expression profiles (GSE66360 and GSE48060 datasets) from human AMI and control samples were downloaded from the GEO database. Differentially expressed genes (DEGs) were screened between 80 AMI and 71 control samples. The LASSO regression model and support vector machine recursive feature elimination (SVM-RFE) analysis were performed to identify candidate biomarkers. The area under the receiver operating characteristic curve (AUC) value was obtained and used to evaluate discriminatory ability. The expression level and diagnostic value of the biomarkers in AMI were further validated in the GSE60993 dataset (17 AMI patients and 7 controls). The compositional patterns of the 22 types of immune cell fraction in AMI were estimated based on the merged cohorts using CIBERSORT. Results: A total of 27 genes were identified. The identified DEGs were mainly involved in carbohydrate binding, Kawasaki disease, atherosclerosis, and arteriosclerotic cardiovascular disease. Gene sets related to atherosclerosis signaling, primary immunodeficiency, IL-17, and TNF signaling pathways were differentially activated in AMI compared with the control. IL1R2, IRAK3, and THBD were identified as diagnostic markers of AMI (AUC = 0.877) and validated in the GSE60993 dataset (AUC = 0.941). Immune cell infiltration analysis revealed that IL1R2, IRAK3, and THBD were correlated with M2 macrophages, neutrophils, monocytes, CD4 + resting memory T cells, activated natural killer (NK) cells, and gamma delta T cells. Conclusion: IL1R2, IRAK3, and THBD can be used as diagnostic markers of AMI, and can provide new insights for future studies on the occurrence and the molecular mechanisms of AMI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction

Zhao

Xie

Zhang

2020

Front. Cardiovasc. Med.

103

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“…SOCS3 increased in the vast majority of patients in the rst days of MI [54]. The mRNA expression levels of the SOCS3 gene in AMI patients was 1.33-fold higher than that in the stable coronary artery disease patients, and the level of the SOCS3 protein was 1.25-fold higher [19]. B-cell lymphoma-2 (BCL2) family proteins, comprising proapoptotic proteins (Bax and Bak), antiapoptotic proteins (BCL2, BCL-XL, BCL-w, MCL1, and A1) and BCL-2 homology domain 3 (BH3)-only proteins (Bid, Noxa, and Puma), have long been identi ed as pivotal apoptosis regulators [55].…”

Section: Discussionmentioning

confidence: 92%

Identification of Common Mechanisms and Key Genes in the Chronic Obstructive Pulmonary Disease and Acute Myocardial Infarction

Chen¹,

Hou²,

Tang³

2021

Preprint

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Background: Chronic obstructive pulmonary disease (COPD) and acute myocardial infarction (AMI) have a strong association. We aimed to study the relationships between COPD and AMI, and reveal potential therapeutic targets and biomarkers. Materials and methods: The dataset GSE38974 and GSE60993 were downloaded from the Gene Expression Omnibus (GEO) database to analyze the intersections among differentially expressed genes (DEGs). Common DEGs were identified and performed functional enrichment analyses. The hub genes were obtained based on the protein-protein interaction (PPI) network by cytoHubba in Cytoscape software. The receiver operator characteristic (ROC) curve analysis was applied to identify the diagnosis efficacy of hub genes. The relationship between hub genes and these two diseases in the CTD database were validated. Finally, the transcription factors (TFs) corresponding to hub genes were also analyzed. Results: In our study, sixty-five common DEGs were obtained in COPD and AMI. GO enrichment analysis indicated that inflammation or apoptotic biological processes are significant enriched biological processes. Common DEGs were mostly enriched in pathways including apoptosis, HIF-1 signaling pathway, TNF signaling pathway, and cytokine-cytokine receptor interaction. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes. Furthermore, we found that the expression of hub genes was significantly associated with a diagnosis efficacy of COPD and AMI. We also validated the relationship between the hub genes and these two diseases in the CTD database. We also found that ELK1, ETV4, STAT3 and TFAP2A were significant TFs, which interacted with the hub genes. Conclusion: In conclusion, our study revealed the communal DEGs and related mechanisms between the pathophysiology of COPD and AMI. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes that are associated with COPD and AMI. Our study provides new ideas and evidence for further exploration of the mechanisms and treatment of COPD and AMI.

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“…The mRNA expression levels of the SOCS3 gene in peripheral blood cells of AMI patients was 1.33-fold higher than that in the stable coronary artery disease (SCAD) patients [19].…”

Section: Socs3mentioning

confidence: 83%

Identification of potential biomarkers and therapeutic targets in the chronic obstructive pulmonary disease and acute myocardial infarction

Chen¹,

Hou²,

Tang³

2021

Preprint

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Background Chronic obstructive pulmonary disease (COPD) and acute myocardial infarction (AMI) have a strong association. We aimed to study the relationships between COPD and AMI, and reveal potential therapeutic targets and biomarkers. , Methods The dataset GSE38974 and GSE60993 were downloaded from the Gene Expression Omnibus (GEO) database to analyze the intersections among differentially expressed genes (DEGs). Common DEGs were identified and performed functional enrichment analyses. The hub genes were obtained based on the protein-protein interaction (PPI) network by cytoHubba in Cytoscape software. The receiver operator characteristic (ROC) curve analysis was applied to identify the diagnosis efficacy of hub genes. The relationship between hub genes and these two diseases in the CTD database were validated. Finally, the transcription factors (TFs) corresponding to hub genes were also analyzed. Results In our study, sixty-five common DEGs were obtained in COPD and AMI. GO enrichment analysis indicated that inflammation or apoptotic biological processes are significant enriched biological processes. Common DEGs were mostly enriched in pathways including apoptosis, HIF-1 signaling pathway, TNF signaling pathway, and cytokine-cytokine receptor interaction. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes. Furthermore, we found that the expression of hub genes was significantly associated with a diagnosis efficacy of COPD and AMI. We also validated the relationship between the hub genes and these two diseases in the CTD database. We also found that ELK1, ETV4, STAT3 and TFAP2A were significant TFs, which interacted with the hub genes. Conclusions In conclusion, our study revealed the communal DEGs and related mechanisms between the pathophysiology of COPD and AMI. MMP9, SOCS3, MCL1, ERBB2 and S100A12 were identified as the hub genes that are associated with COPD and AMI. Our study provides new ideas and evidence for further exploration of the mechanisms and treatment of COPD and AMI.

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High Expression Levels of the SOCS3 Gene Are Associated with Acute Myocardial Infarction

Cited by 16 publications

References 37 publications

Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction

Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction

Identification of Common Mechanisms and Key Genes in the Chronic Obstructive Pulmonary Disease and Acute Myocardial Infarction

Identification of potential biomarkers and therapeutic targets in the chronic obstructive pulmonary disease and acute myocardial infarction

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High Expression Levels of the SOCS3 Gene Are Associated with Acute Myocardial Infarction

Cited by 16 publications

References 37 publications

Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction

Predicting Diagnostic Gene Biomarkers Associated With Immune Infiltration in Patients With Acute Myocardial Infarction

Identification of&nbsp;Common Mechanisms and Key Genes in the Chronic Obstructive Pulmonary Disease and Acute Myocardial Infarction

Identification of potential biomarkers and therapeutic targets in the chronic obstructive pulmonary disease and acute myocardial infarction

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Identification of Common Mechanisms and Key Genes in the Chronic Obstructive Pulmonary Disease and Acute Myocardial Infarction