The Association of IL-6, TNFα and CRP Gene Polymorphisms with Coronary Artery Disease in a Tunisian Population: A Case–Control study

Grira, Nedra; Lahidheb, Dhaker; Lamine, Oussama; Ayoub, Manel; Wassaifi, Souhir; Aouni, Z.; Fehri, Wafa; Mazigh, C.

doi:10.1007/s10528-021-10035-0

Cited by 3 publications

(3 citation statements)

References 38 publications

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“…Figure 3 b displays the semantic-triples connections between glycine and coronary heart disease after searching for enriched overlapping terms. A total of 73 overlapping terms was identified, including homocysteine [ 51 , 52 , 53 ], ethanol [ 54 , 55 ] and TNF protein [ 56 , 57 ]. In the case of homocysteine, “homocysteine—PREDISPOSES—Coronary Arteriosclerosis” is the most enriched semantic triple on the outcome side ( p -value: 4.38 × 10 −120 ), whereas “Glycine—INTERACTS_WITH—homocysteine” has a p -value of 8.3 × 10 −6 .…”

Section: Resultsmentioning

confidence: 99%

mGWAS-Explorer 2.0: Causal Analysis and Interpretation of Metabolite–Phenotype Associations

2023

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Metabolomics-based genome-wide association studies (mGWAS) are key to understanding the genetic regulations of metabolites in complex phenotypes. We previously developed mGWAS-Explorer 1.0 to link single-nucleotide polymorphisms (SNPs), metabolites, genes and phenotypes for hypothesis generation. It has become clear that identifying potential causal relationships between metabolites and phenotypes, as well as providing deep functional insights, are crucial for further downstream applications. Here, we introduce mGWAS-Explorer 2.0 to support the causal analysis between >4000 metabolites and various phenotypes. The results can be interpreted within the context of semantic triples and molecular quantitative trait loci (QTL) data. The underlying R package is released for reproducible analysis. Using two case studies, we demonstrate that mGWAS-Explorer 2.0 is able to detect potential causal relationships between arachidonic acid and Crohn’s disease, as well as between glycine and coronary heart disease.

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Section: Resultsmentioning

confidence: 99%

mGWAS-Explorer 2.0: Causal Analysis and Interpretation of Metabolite–Phenotype Associations

2023

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“…(2021 г. ), исследовав популяцию Туниса, определили высокую частоту встречаемости АА-генотипа в группе пациентов с острым коронарным синдромом с подъемом сегмента ST (16,7%) по сравнению с таковым без подъема ST-сегмента (9,7%) и пациентов со стабильной стенокардией (11,5%) [35].…”

Section: ассоциация полиморфизма Rs1800629 гена Tnf с имunclassified

Tumor necrosis factor gene polymorphism rs1800629 in patients with atherosclerotic cardiovascular diseases: A review

Khazova,

Bulashova,

Valeeva

2023

Consilium Medicum

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The close attention of researchers is riveted to the study of socially significant multifactorial diseases and syndromes with a hereditary predisposition, which include chronic heart failure, formed as a result of atherosclerosis of the coronary arteries. The promise of genomic studies in atherosclerosis and heart failure is associated with the possibility of determining the genetic risk of developing and predicting adverse cardiovascular events before the onset of clinical signs/symptoms. From the standpoint of understanding the pathogenesis of atherosclerosis as a variant of nonspecific inflammation, which has a wave-like character, it is assumed that genes encoding pro-inflammatory cytokines influence the pathological process. The aim of the review was to analyze the results of studies available in available publications on the rs1800629 polymorphism of the tumor necrosis factor (TNF) gene in patients with atherosclerotic cardiovascular diseases. Most data indicate the presence of an increased cardiovascular risk in carriers of the A allele of the rs1800629 polymorphism of the TNF gene. It was determined that carriage of the AA genotype is associated with essential arterial hypertension and remodeling of the left ventricular myocardium. In patients with chronic heart failure with preserved and moderately reduced left ventricular ejection fraction of the AA genotype, low blood pressure and frequent occurrence of atrial fibrillation were noted. A number of papers present the results of studies of the rs1800629 polymorphism of the TNF gene and the prognostic significance of the rs1800629 polymorphism of the TNF gene in heart failure.

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“…rs1800629 (also known as -308 G > A), is located in the promoter at position -308, formed by substitution from guanine (G) to adenine (A), resulting in a 2–3 time increase in the transcriptional activity of TNF-α [ 34 ]. In addition to the rs1800795 C allele and the rs1800629 A allele may elevate plasma levels of C-reactive protein (CRP) [ 35 , 36 ], it indicates that pro-inflammatory cytokines variants (i.e., 1800795 and rs1800629) may impact systemic inflammatory profile (i.e., IL-6, TNF-α, and CRP). Here, we conducted this study to investigate this hypothesis.…”

Section: Introductionmentioning

confidence: 99%

Impacts of Inflammatory Cytokines Variants on Systemic Inflammatory Profile and COVID-19 Severity

Deng,

Tang,

Wang

et al. 2024

J Epidemiol Glob Health

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Background Cytokine storm is known to impact the prognosis of coronavirus disease 2019 (COVID-19), since pro-inflammatory cytokine variants are associated with cytokine storm. It is tempting to speculate that pro-inflammatory cytokines variants may impact COVID-19 outcomes by modulating cytokine storm. Here, we verified this hypothesis via a comprehensive analysis. Methods PubMed, Cochrane Library, Central, CINAHL, and ClinicalTrials.gov were searched until December 15, 2023. Case–control or cohort studies that investigated the impacts of rs1800795 or rs1800629 on COVID-19 susceptibility, severity, mortality, IL-6, TNF-α, or CRP levels were included after an anonymous review by two independent reviewers and consultations of disagreement by a third independent reviewer. Results 47 studies (8305 COVID-19 individuals and 17,846 non-COVID-19 individuals) were analyzed. The rs1800629 A allele (adenine at the −308 position of the promoter was encoded by the A allele) was associated with higher levels of tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP). In contrast, the rs1800795 C allele (cytosine at the −174 position of the promoter was encoded by the C allele) was linked to higher levels of interleukin-6 (IL-6) and CRP. In addition, the A allele of rs1800629 increased the severity and mortality of COVID-19. However, the C allele of rs1800795 only increased COVID-19 susceptibility. Conclusions rs1800629 and rs1800795 variants of pro-inflammatory cytokines have significant impacts on systemic inflammatory profile and COVID-19 clinical outcomes. rs1800629 may serve as a genetic marker for severe COVID-19.

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The Association of IL-6, TNFα and CRP Gene Polymorphisms with Coronary Artery Disease in a Tunisian Population: A Case–Control study

Cited by 3 publications

References 38 publications

mGWAS-Explorer 2.0: Causal Analysis and Interpretation of Metabolite–Phenotype Associations

mGWAS-Explorer 2.0: Causal Analysis and Interpretation of Metabolite–Phenotype Associations

Tumor necrosis factor gene polymorphism rs1800629 in patients with atherosclerotic cardiovascular diseases: A review

Impacts of Inflammatory Cytokines Variants on Systemic Inflammatory Profile and COVID-19 Severity

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