ArticleHeart and vessels2008
Synergistic effects between 561A > C and 98G > T polymorphisms of E-selectin gene and hypercholesterolemia in determining the susceptibility to coronary artery disease.
Article in Heart and vessels, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 5 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 5 syntheses or guidelines pooled it, 23 citations in OpenAlex.
- Pooled it
- Correlations of SELE and SELP genetic polymorphisms with myocardial infarction risk: a meta-analysis and meta-regression.Molecular biology reports · 2014Pooled it
- Correlations of SELE genetic polymorphisms with risk of coronary heart disease and myocardial infarction: a meta-analysis.Molecular biology reports · 2014Pooled it
- Heterogeneous effect of two selectin gene polymorphisms on coronary artery disease risk: a meta-analysis.PloS one · 2014Pooled it
- Association of A561C and G98T polymorphisms in E-selectin gene with coronary artery disease: a meta-analysis.PloS one · 2013Pooled it
- Evaluation of Plasma E-Selectin Concentration as a Risk Marker for Atherosclerotic Vascular Damage in Patients with Early CAD.Biomolecules · 2024Article
- Association of rs5368 and rs3917406 polymorphisms in E-selectin gene with premature coronary artery disease in Chinese Han population.International journal of clinical and experimental medicine · 2015Article
- Assessment of the E-selectin rs5361 (561A>C) polymorphism and soluble protein concentration in acute coronary syndrome: association with circulating levels.Mediators of inflammation · 2014Article
- Low frequency haplotypes of E-selectin polymorphisms G2692A and C1901T give increased protection from coronary artery disease.Medical science monitor : international medical journal of experimental and clinical research · 2011Article
- Two single nucleotide polymorphisms in ALOX15 are associated with risk of coronary artery disease in a Chinese Han population.Heart and vessels · 2010Article
- Association of the CYBA, PPARGC1A, PPARG3, and PPARD gene variants with coronary artery disease and metabolic risk factors of coronary atherosclerosis in a Russian population.Heart and vessels · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary artery disease (CAD) is a multifactorial disease that results from the interaction between genetic and traditional risk factors. The endothelium dysfunction plays a key role in the progression of atherosclerotic lesions. E-selectin is a marker of endothelium dysfunction. The aim of the present study was to find a relationship between 561A > C and 98G > T polymorphisms of E-selectin gene and CAD as well as interactions between these polymorphic variants and traditional risk factors of the disease in determining the susceptibility to CAD. The study population included 191 patients with angiographically documented CAD and 203 blood donors. The analysis of genetic polymorphisms was performed using the polymerase chain reaction-restriction fragment length polymorphism method. We found that the frequencies of 561C and 98T alleles of E-selectin gene and carriers of C and T alleles were similar in the entire groups as well as in the age-and sex-matched subgroups. We observed a strong significant correlation between those two polymorphisms; almost all subjects possessing one "proatherosclerotic" allele of E-selectin gene also had the second allele (r = 0.963, P < 0.0001). There were also synergistic effects between both polymorphisms and hypercholesterolemia (but not with smoking or overweight) in determining the susceptibility to CAD. The present study points to synergistic interactions between 561A > C or 98G > T polymorphisms of E-selectin gene and hypercholesterolemia that cause a significant increase in the susceptibility to CAD.
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