Association of genetic polymorphisms in vascular endothelial growth factor with susceptibility to coronary artery disease: a meta–analysis

Ma, Wen-Qi; Wang, Ying; Han, Xi‐Qiong; Zhu, Yi; Liu, Naifeng

doi:10.1186/s12881-018-0628-3

Cited by 15 publications

(10 citation statements)

References 45 publications

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“…The characterization of genetic polymorphisms of the VEGFA gene that influence the gene's expression [3,4] and the central role of VEGF-A in blood vessel formation have made the gene an object of interest in studies of susceptibility to, and progression of, cardiovascular disease [34,35]. We found one of three SNPs assayed, rs699947, was an independent predictor of mortality in male non-diabetic participants in the CDCS cohort.…”

Section: Discussionmentioning

confidence: 86%

Vascular endothelial growth factor-A promoter polymorphisms, circulating VEGF-A and survival in acute coronary syndromes

et al. 2021

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Background Development of a competent collateral circulation in established coronary artery disease is cardio-protective. The vascular endothelial growth factor (VEGF) system plays a key role in this process. We investigated the prognostic performance of circulating VEGF-A and three genetic variants in the VEGFA gene in a clinical coronary cohort. Methods and results The Coronary Disease Cohort Study (CDCS) recruited 2,140 patients, with a diagnosis of acute coronary syndrome (ACS), after admission to Christchurch or Auckland City Hospitals between July 2002 and January 2009. We present data for 1927 patients from the cohort genotyped for three SNPs in the VEGF-A gene, rs699947 (C-2578A), rs2010963 (C405G) and rs3025039 (C936T). Plasma VEGF-A concentrations were assayed in a subgroup (n = 550) of CDCS patients (geometric mean 36.6 [34.7–38.5] pg/ml). VEGF-A levels correlated with patient heart rate at baseline (p = 0.034). None of rs699947, rs3025039, nor rs2010963 genotypes were significantly associated with VEGF-A levels, but rs3025039 genotype was positively associated with collateral vessels perfusion according to the Rentrop classification (p = 0.01) and baseline natriuretic peptide levels (p<0.05). Survival in the CDCS cohort was independently associated with baseline VEGF-A levels and (in males) with rs699947 genotype. Conclusions This study is strongly suggestive that VEGF-A levels have value as a prognostic biomarker in coronary heart disease patients and SNPs in VEGF-A deserve further investigation as prognostic markers and indicators of angiogenic potential influencing the formation of collateral circulation.

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Section: Discussionmentioning

confidence: 86%

Vascular endothelial growth factor-A promoter polymorphisms, circulating VEGF-A and survival in acute coronary syndromes

et al. 2021

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“…In particular, VEGF gene variability may be important for several angiogenesis-associated diseases, such as tumors or coronary disease [56]. Hyper-activation of the VEGFA pathway and an excess of deleterious variants in VEGFA and VEGFA pathway genes have been found to be associated with ASDs and TF [23,24,57].…”

Section: Discussionmentioning

confidence: 99%

Susceptibility to Heart Defects in Down Syndrome Is Associated with Single Nucleotide Polymorphisms in HAS 21 Interferon Receptor Cluster and VEGFA Genes

Balistreri

Ammoscato

Scola

et al. 2020

Genes

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Background: Congenital heart defects (CHDs) are present in about 40–60% of newborns with Down syndrome (DS). Patients with DS can also develop acquired cardiac disorders. Mouse models suggest that a critical 3.7 Mb region located on human chromosome 21 (HSA21) could explain the association with CHDs. This region includes a cluster of genes (IFNAR1, IFNAR2, IFNGR2, IL10RB) encoding for interferon receptors (IFN-Rs). Other genes located on different chromosomes, such as the vascular endothelial growth factor A (VEGFA), have been shown to be involved in cardiac defects. So, we investigated the association between single nucleotide polymorphisms (SNPs) in IFNAR2, IFNGR2, IL10RB and VEGFA genes, and the presence of CHDs or acquired cardiac defects in patients with DS. Methods: Individuals (n = 102) with DS, and age- and gender-matched controls (n = 96), were genotyped for four SNPs (rs2229207, rs2834213, rs2834167 and rs3025039) using KASPar assays. Results: We found that the IFNGR2 rs2834213 G homozygous genotype and IL10RB rs2834167G-positive genotypes were more common in patients with DSand significantly associated with heart disorders, while VEGFA rs3025039T-positive genotypes (T/*) were less prevalent in patients with CHDs. Conclusions: We identified some candidate risk SNPs for CHDs and acquired heart defects in DS. Our data suggest that a complex architecture of risk alleles with interplay effects may contribute to the high variability of DS phenotypes.

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“…After referring to several reported meta-analyses [25–27], we utilized STATA 12.0 software (Stata Corporation, College Station, TX, USA) to conduct the I 2 test and Q statistic test (for heterogeneity evaluation), DerSimonian-Laird and Mantel-Haenszel method (for association test), Begg’s test and Egger’s test (for publication bias evaluation) [28, 29], and sensitivity analysis (for the assessment of data stability). The high heterogeneity level was considered to perform the DerSimonian-Laird method under a random-effect model when I 2 was larger than 50% or the P value was less than 0.05.…”

Section: Methodsmentioning

confidence: 99%

Genetic relationship between IL-10 gene polymorphisms and the risk of clinical atopic dermatitis

Kong

2019

BMC Med Genet

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Background We retrieved different reports containing different genetic effects of − 1082 A/G, − 819 T/C, and − 592 A/C polymorphisms within the IL-10 (interleukin-10) gene on the susceptibility to clinical atopic dermatitis. Methods Herein, we conducted a meta-analysis to comprehensively assess such a genetic relationship after collecting the available published evidence. STATA 12.0 software was used for the statistical analysis under the allelic, homozygotic, heterozygotic, dominant, recessive and carrier genetic models. Results By retrieving and screening database literature, a total of 16 eligible case-control studies were finally selected. For the IL-10 -1082 A/G polymorphism, we did not detect a significant difference between atopic dermatitis cases and population-based controls in the overall meta-analysis under the genetic models of allele G vs. A ( P = 0.540), GG vs. AA ( P = 0.853), AG vs AA ( P = 0.265), AG + GG vs AA ( P = 0.221), GG vs AA+AG ( P = 0.540) and carrier G vs. A ( P = 0.643). Moreover, a statistically non-significant association was observed in the most subgroup meta-analyses by the factors of ethnicity, country and Hardy-Weinberg equilibrium. Likewise, the negative results were detected for the synthetic analysis of IL-10 -819 T/C and − 592 C/A polymorphisms. Conclusion The current evidence does not support a strong genetic relationship between IL-10 -1082 A/G, − 819 T/C and − 592 A/C polymorphisms and the susceptibility to atopic dermatitis. Electronic supplementary material The online version of this article (10.1186/s12881-019-0817-8) contains supplementary material, which is available to authorized users.

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Association of genetic polymorphisms in vascular endothelial growth factor with susceptibility to coronary artery disease: a meta–analysis

Cited by 15 publications

References 45 publications

Vascular endothelial growth factor-A promoter polymorphisms, circulating VEGF-A and survival in acute coronary syndromes

Vascular endothelial growth factor-A promoter polymorphisms, circulating VEGF-A and survival in acute coronary syndromes

Susceptibility to Heart Defects in Down Syndrome Is Associated with Single Nucleotide Polymorphisms in HAS 21 Interferon Receptor Cluster and VEGFA Genes

Genetic relationship between IL-10 gene polymorphisms and the risk of clinical atopic dermatitis

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