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

2021 ◽  
Author(s):  
Lijie Wang ◽  
Fengxia Yu
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Signal Transduction ◽  
Transcription Factors ◽  
Expression Analysis ◽  
Transport Processes ◽  
Functional Enrichment ◽  
Hypergeometric Test ◽  
Non Coding Rna ◽  
Patient Consent

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. We constructed a multi-regulator driven dysfunction module for AMI. 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, we obtained a set of expression disorder modules related to AMI. 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: We obtained 4551 differentially expressed genes for AMI and seven co-expression modules. 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, we revealed 3 of 24 transcription factors (TFs) including NFKB1, MECP2 and SIRT1, 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, we used a dysfunction module 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.Trial registration: All analyses were based on previous study, thus no ethical approval and patient consent are required. The dataset of GSE48060 is from GEO and the accession number is PRJNA208840.

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

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Lijie Wang ◽  
Fengxia Yu
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Signal Transduction ◽  
Transcription Factors ◽  
Expression Analysis ◽  
Dna Recombination ◽  
Transport Processes ◽  
Functional Enrichment ◽  
Hypergeometric Test ◽  
Non Coding Rna

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.

scholarly journals Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
D. Julia Trembinski ◽  
Diewertje I. Bink ◽  
Kosta Theodorou ◽  
Janina Sommer ◽  
Ariane Fischer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Non Coding Rna ◽  
Long Non Coding Rna

EARLY EXPRESSION OF CIRCULATING LONG NON-CODING RNA CORRELATES WITH THE RISK OF 1-YEAR MORTALITY AFTER ACUTE MYOCARDIAL INFARCTION

2020 ◽  
Vol 75 (11) ◽  
pp. 186
Author(s):  
Perman Pandal ◽  
Aaron Shulkin ◽  
Eliseo Vazquez ◽  
Elizabeth Cortez-Toledo ◽  
Diana Ramos ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Non Coding Rna ◽  
Early Expression ◽  
Long Non Coding Rna

scholarly journals LncRNA SNHG8 is identified as a key regulator of acute myocardial infarction by RNA-seq analysis

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Liu-An Zhuo ◽  
Yi-Tao Wen ◽  
Yong Wang ◽  
Zhi-Fang Liang ◽  
Gang Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Roc Curve ◽  
Regulatory Networks ◽  
Pairwise Comparison ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Diagnostic Value ◽  
Functional Enrichment ◽  
Rna Seq

Abstract Background Long noncoding RNAs (lncRNAs) are involved in numerous physiological functions. However, their mechanisms in acute myocardial infarction (AMI) are not well understood. Methods We performed an RNA-seq analysis to explore the molecular mechanism of AMI by constructing a lncRNA-miRNA-mRNA axis based on the ceRNA hypothesis. The target microRNA data were used to design a global AMI triple network. Thereafter, a functional enrichment analysis and clustering topological analyses were conducted by using the triple network. The expression of lncRNA SNHG8, SOCS3 and ICAM1 was measured by qRT-PCR. The prognostic values of lncRNA SNHG8, SOCS3 and ICAM1 were evaluated using a receiver operating characteristic (ROC) curve. Results An AMI lncRNA-miRNA-mRNA network was constructed that included two mRNAs, one miRNA and one lncRNA. After RT-PCR validation of lncRNA SNHG8, SOCS3 and ICAM1 between the AMI and normal samples, only lncRNA SNHG8 had significant diagnostic value for further analysis. The ROC curve showed that SNHG8 presented an AUC of 0.850, while the AUC of SOCS3 was 0.633 and that of ICAM1 was 0.594. After a pairwise comparison, we found that SNHG8 was statistically significant (PSNHG8-ICAM1 = 0.002; PSNHG8-SOCS3 = 0.031). The results of a functional enrichment analysis of the interacting genes and microRNAs showed that the shared lncRNA SNHG8 may be a new factor in AMI. Conclusions Our investigation of the lncRNA-miRNA-mRNA regulatory networks in AMI revealed a novel lncRNA, lncRNA SNHG8, as a risk factor for AMI and expanded our understanding of the mechanisms involved in the pathogenesis of AMI.

scholarly journals Identification of monocyte-associated genes as predictive biomarkers of heart failure after acute myocardial infarction

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Qixin Chen ◽  
Qijin Yin ◽  
Junxian Song ◽  
Chuanfen Liu ◽  
Hong Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Rna Sequencing ◽  
Mononuclear Cells ◽  
Characteristic Curve ◽  
Predictive Biomarkers ◽  
Functional Enrichment ◽  
Sequencing Data ◽  
Hub Genes

Abstract Background Acute myocardial infarction (AMI) is a major contributor of heart failure (HF). Peripheral blood mononuclear cells (PBMCs), mainly monocytes, are the essential initiators of AMI-induced HF. The powerful biomarkers for early identification of AMI patients at risk of HF remain elusive. We aimed to identify monocyte-related critical genes as predictive biomarkers for post-AMI HF. Methods We performed weighted gene co-expression network analysis (WGCNA) on transcriptomics of PBMCs from AMI patients who developed HF or did not. Functional enrichment analysis of genes in significant modules was performed via Metascape. Then we obtained the single-cell RNA-sequencing data of recruited monocytes/macrophages from AMI and control mice using the Scanpy and screened 381 differentially expressed genes (DEGs) between the two groups. We validated the expression changes of the 25 genes in cardiac macrophages from AMI mice based on bulk RNA-sequencing data and PBMCs data mentioned above. Results In our study, the results of WGCNA showed that two modules containing 827 hub genes were most significantly associated with post-AMI HF, which mainly participated in cell migration, inflammation, immunity, and apoptosis. There were 25 common genes between DEGs and hub genes, showing close relationship with inflammation and collagen metabolism. CUX1, CTSD and ADD3 exhibited consistent changes in three independent studies. Receiver operating characteristic curve analysis showed that each of the three genes had excellent performance in recognizing post-AMI HF patients. Conclusion Our findings provided a set of three monocyte-related biomarkers for the early prediction of HF development after AMI as well as potential therapeutic targets of post-AMI HF.

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