<i>IL18</i>-family Genes Polymorphism Is Associated with the Risk of Myocardial Infarction and IL18 Concentration in Patients with Coronary Artery Disease

Понасенко, А. В.; Цепокина, А. В.; Khutornaya, M. V.; Sinitsky, M. Yu.; Барбараш, О. Л.

doi:10.1080/08820139.2021.1876085

Cited by 10 publications

(4 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IRF1 (interferon regulatory factor 1) was downregulated by smoking, possibly altering the balance of interferon responses. IL18RAP (interleukin 18 receptor accessory protein) is another noteworthy transcript downregulated in smokers, which plays a role in IBD [ 33 ], lupus, and coronary artery disease [ 34 ]. The Monica Risk, Genetics, Archiving and Monograph (MORGAM) project links proinflammatory IL-18 synthesis with exposure to nicotine [ 35 , 36 ], while the loss of IRF1 impairs interferon-γ-mediated cell signaling in monocytes of smokers [ 37 ].…”

Section: Cd4 + Cells (Helper T Lymphocytes)mentioning

confidence: 99%

Immune cell-specific smoking-related expression characteristics are revealed by re-analysis of transcriptomes from the CEDAR cohort

Nowak¹,

Dybska²,

Adams³

et al. 2022

cejoi

View full text Add to dashboard Cite

Introduction: smoking is known to affect whole-blood expression and methylation profiles. although whole-genome methylation studies indicated that effects observed in blood may be driven by changes within leukocyte subtypes, these phenomena have not been explored using expression profiling.Material and methods: this study reanalyzed data from the Correlated Expression and Disease association research (CEDar) patient cohort recruited by momozawa et al. (E-mtab-6667). Data from gene expression profiling of immunomagnetically sorted CD4 + , CD8 + , CD14 + , CD15 + , and CD19 + cells were processed. Differential expression analyses were conducted in each immune cell type, followed by gene ontology analysis and supplementary investigations.Results: ninety-four differentially expressed genes were found (CD8 + n = 58, CD14 + n = 20, CD4 + n = 14, CD19 + n = 2). two key smoking-related genes were overexpressed in specific cell types: lrrn3 (CD4 + , CD8 + ) and mmP25 (CD8 + , CD14 + ). in CD4 + cells smoking was associated with reduced expression of the nK cell receptor Klrb1, suggesting CD4 + subpopulation shifts and differences in interferon signaling (reduced irf1 and il18raP in smokers). Key results and their integration with an immune protein-protein interaction network revealed that smoking influences integrins in CD8 + cells (itGb7, itGal, itGam, itGb2). C-type lectin ClEC4a was reduced in CD8 + cells and ClEC10a was increased in CD14 + cells from smokers; moreover, ClEC5a (CD8 + ), ClEC7a (CD8 + ) and ClEC9a (CD19 + ) were related to smoking in supplementary analyses. CD14 + cells from smokers exhibited overexpression of lDlr and the formyl peptide receptor fPr3.Conclusions: smoking specifically alters vital immune regulation genes in lymphocyte subtypes, especially CD4 + , CD8 + and CD14 + cells.

show abstract

Section: Cd4 + Cells (Helper T Lymphocytes)mentioning

confidence: 99%

Immune cell-specific smoking-related expression characteristics are revealed by re-analysis of transcriptomes from the CEDAR cohort

Nowak¹,

Dybska²,

Adams³

et al. 2022

cejoi

View full text Add to dashboard Cite

show abstract

“…Since CAE is related with inflammation and usually coexists with CAD, it has been hypothesised that CAE is a subtype of CAD. On the basis of the results of earlier investigations, it has been hypothesised that a more severe inflammation may play a role in the aetiology of CAE [16].…”

Section: Discussionmentioning

confidence: 99%

Coronary Artery Ectasia as a Predictor of Major Adverse Cardiac Events in Patients with Acute ST Elevation Myocardial Infarction

Saad

Gaafar²,

Salama³

et al. 2023

View full text Add to dashboard Cite

Background: Coronary artery ectasia (CAE) is characterised as localised or widespread non-obstructive lesions of the epicardial coronary arteries with a luminal dilation more than 1.5 times the neighbouring normal segments or vessel diameter. Isolated CAE is CAE in the absence of severe coronary artery stenosis. This aberrant dilatation of coronary arteries can produce angina pectoris and even myocardial infarction in people without coronary artery disease owing to vasospasm, dissection, or thrombus. The purpose of this study was to evaluate the connection between CAE and major adverse cardiac events (MACE) following acute myocardial infarction with ST elevation. Methods: This was a prospective cohort study which was carried out on 300 cases. Cases were divided into two groups: Group I: including about 22 STEMI cases with CAE and Group II: including about 278 STEMI cases without CAE. All cases in this study were subjected to full history taking, clinical examination, laboratory tests, standard 12-leads ECG, resting transthoracic echocardiography (TTE), and coronary angiography. Results: Regarding MACE in the studied groups, Incidence of reinfarction and cardiac death were significant higher in cases with STEMI and CAE than cases with STEMI alone. In univariate regression analysis, CAE (OR: 3.59, p value =0.022) was a significant predictor of cardiac death but age, male sex, and EF were not. Also, in multivariate regression analysis CAE (OR: 3.49, p value =0.029) was a significant predictor of cardiac death but age, male sex, and EF were not smoking with high warfarin consumption. Further, Markis classification 1 and 3 were the most frequent phenotype among cases. In STEMI cases, the incidence of reinfarction and cardiac death were significantly higher in cases with STEMI and CAE than cases with STEMI alone. So, CAE is a significant predictor of cardiac death.

show abstract

“…PLA2G2A [61], CCL23 [62], CD53 [63], TREML4 [64], TREM2 [65], CD180 [66], HPSE (heparanase) [67], CELA2A [68], TNFRSF4 [69], AMBP (alpha-1-microglobulin/bikunin precursor) [70], SOX18 [71], PANX2 [72], RSPO2 [73], COMP (cartilage oligomeric matrix protein) [74], ASGR1 [75] and NOXA1 [76] are involved in progression of atherosclerosis. A previous study reported that S100A9 [77], ADORA3 [78], IL1R2 [79], FPR1 [80], CCL20 [81], CD163 [82], S100A8 [83], TLR2 [84], HAS2 [85], PTX3 [86], TIMP4 [87], AREG (amphiregulin) [88], LBP (lipopolysaccharide binding protein) [89], IL18R1 [90], ALOX5AP [91], RETN (resistin) [92], F13A1 [93], FPR2 [94], SAA1 [95], FLT3 [96], AQP4 [97], FCER1G [98], CCL18 [99], HP (haptoglobin) [100], CDK1 [101], SLC7A11 [102], CFTR (CF transmembrane conductance regulator) [103], F8 [104], STC1[44], IL18RAP [90], TIMP3 [105], PDE4D [106], CYP4A11 [107], SCN10A [108], APOB (apolipoprotein B) [109], ACE (angiotensin I converting enzyme) [110], PENK (proenkephalin) [111], HSPB6 [112], TLR9 [113], EGR1 [114], CACNG8 [115], FOXD3 [116], DBH (dopamine beta-hydroxylase) [117], FOXP3 [118], GLP1R [119], IL34 [120], CCN1 [121], ADRA2A [122], BGN (biglycan) [123], NOS2 [124], AGRN (agrin) [125], DRD1 [126], GNB3 [127], EGR2 [128], MDK (midkine) [129], NOTCH3 [130], AZIN2 [131], NOTCH1 [132], LOX...…”

Section: Discussionmentioning

confidence: 99%

Identification and Interaction Analysis of Molecular Markers in Myocardial Infarction by Integrated Bioinformatics Analysis

Vastrad¹,

Vastrad²

2021

Preprint

View full text Add to dashboard Cite

Myocardial infarction (MI) is the leading cardiovascular diseases in worldwide, yet relatively little is known about the genes and signaling pathways involved in MI progression. The present investigation aimed to elucidate potential crucial candidate genes and pathways in MI. expression profiling by high throughput sequencing dataset (GSE132143) was downloaded from the Gene Expression Omnibus (GEO) database, which included data from 20 MI samples and 12 normal control samples. Differentially expressed genes (DEGs) were identified using t-tests in the DESeq2 R package. These DEGs were subsequently investigated by Gene Ontology (GO) and pathway enrichment analysis, a protein-protein interaction (PPI) network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed and analyzed. Hub genes were validated by receiver operating characteristic curve (ROC) analysis. In total, 958 DEGs were identified, of which 480 were up regulated and 478 were down regulated. GO and pathway enrichment analysis results revealed that the DEGs were mainly enriched in, immune system, neuronal system, response to stimulus, and multicellular organismal process. A PPI network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network was constructed by using Cytoscape software, and CFTR, CDK1, RPS13, RPS15A, RPS27, NOTCH1, MRPL12, NOS2, CCDC85B and ATN1 were identified as the hub genes. Our results highlight the important roles of the genes including CFTR, CDK1, RPS13, RPS15A, RPS27, NOTCH1, MRPL12, NOS2, CCDC85B and ATN1 in MI pathogenesis or therapeutic management.

show abstract

IL18-family Genes Polymorphism Is Associated with the Risk of Myocardial Infarction and IL18 Concentration in Patients with Coronary Artery Disease

Cited by 10 publications

References 49 publications

Immune cell-specific smoking-related expression characteristics are revealed by re-analysis of transcriptomes from the CEDAR cohort

Immune cell-specific smoking-related expression characteristics are revealed by re-analysis of transcriptomes from the CEDAR cohort

Coronary Artery Ectasia as a Predictor of Major Adverse Cardiac Events in Patients with Acute ST Elevation Myocardial Infarction

Identification and Interaction Analysis of Molecular Markers in Myocardial Infarction by Integrated Bioinformatics Analysis

Contact Info

Product

Resources

About