scholarly journals Association of c.56C > G (rs3135506) Apolipoprotein A5 Gene Polymorphism with Coronary Artery Disease in Moroccan Subjects: A Case-Control Study and an Updated Meta-Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Imane Morjane ◽  
Hicham Charoute ◽  
Sanaa Ouatou ◽  
Lamiae Elkhattabi ◽  
Houda Benrahma ◽  
...  

Purpose. Coronary artery diseases (CAD) are clinical cardiovascular events associated with dyslipidemia in common. The interaction between environmental and genetic factors can be responsible for CAD. The present paper aimed to examine the association between c.56C > G (rs3135506) APOA5 gene polymorphism and CAD in Moroccan individuals and to perform an association update meta-analysis. Materials and Methods. The c.56C > G variant was genotyped in 122 patients with CAD and 134 unrelated controls. Genetic association analysis and comparison of biochemical parameters were performed using R statistical language. In addition, a comprehensive meta-analysis including eleven published studies in addition to our case-control study results was conducted using Review Manager 5.3. Publication bias was examined by Egger’s test and funnel plot. Results. The case-control study data showed that the c.56C > G polymorphism was associated with CAD susceptibility under codominant (P-value = 0.001), recessive (P-value <0.001) and log-additive (P-value = 0.008) inheritance models. In addition, this polymorphism was significantly associated with increased levels of systolic and diastolic blood pressures, triglycerides, glycemia, and total cholesterol. Furthermore, meta-analysis showed a significant association between the c.56C > G gene polymorphism and increased risk of CAD under recessive (OR = 3.39[1.77–6.50], P value <0.001) and homozygote codominant (OR = 3.96[2.44–6.45], P value <0.001) models. Conclusion. Our case-control study revealed a significant association between c.56C > G polymorphism and CAD in the Moroccan population. In addition, meta-analysis data supported the implication of this polymorphism in CAD susceptibility.

Cytokine ◽  
2021 ◽  
Vol 139 ◽  
pp. 155403
Author(s):  
Marzieh Ghalandari ◽  
Khadijeh Jamialahmadi ◽  
Maryam Mardan Nik ◽  
Maryam Pirhoushiaran ◽  
Seyed Reza Mirhafez ◽  
...  

2020 ◽  
Vol 8 (F) ◽  
pp. 197-202
Author(s):  
I Putu Yuda Prabawa ◽  
Anak Agung Wiradewi Lestari ◽  
I Made Muliarta ◽  
Putu Eka Mardhika ◽  
Gusti Ayu Riska Pertiwi ◽  
...  

BACKGROUND: Single-nucleotide polymorphism in the stromal cell-derived factor-1 (SDF-1)/CXCL12 gene had been associated with an increased risk of coronary artery disease (CAD). However, several published studies have shown inconsistent results. AIM: A meta-analysis was assessed to evaluate the association between SDF-1 3’A-gene polymorphism and CAD in the literature. METHODS: A systematic review was conducted in accordance with PRISMA guidelines and adhering to the Cochrane Handbook for Systematic Reviews. The literature search strategy was carried out on April 3, 2019, from PubMed, EBSCO, Google Scholar, and DOAJ during 2013–2018 period using various keywords related to SDF-1, CXCL12, polymorphism, and CAD. Original data from the group, case-control study, English full-text, and DNA polymorphism assessment using polymerase chain reaction were enrolled. Gene polymorphism in A-base nucleotide among patients with CAD and healthy subjects were evaluated. All data were analyzed using Review Manager 5.3 (Cochrane, Denmark) for meta-analysis. RESULTS: Five eligible studies extracted for data analysis (2013–2018) based on the assessment of 2-independent reviewers. Several studies have been excluded due to irrelevant criteria evaluated. A significant result was found between SDF-1 3’A gene polymorphism with the increased risk of CAD in the overall effect evaluation using a fixed-effects model (odds ratio [OR]: 2.02; 95% confidence interval 1.54-2.65; I2: 34%; p<0.001) on the forest plot. CONCLUSION: Our meta-analysis suggests that gene polymorphism in A-base nucleotide of SDF-1/CXCL-12 was associated with the susceptibility of CAD. However, a bigger-scale and well-design of case-control study should be conducted to clarify these conclusions.


2011 ◽  
Vol 39 (5) ◽  
pp. 5269-5276 ◽  
Author(s):  
Changwei Tian ◽  
Tongtao Liu ◽  
Shengxia Fang ◽  
Xunbo Du ◽  
Chongqi Jia

2010 ◽  
Vol 163 (3) ◽  
pp. 427-434 ◽  
Author(s):  
José Miguel Dora ◽  
Walter Escouto Machado ◽  
Jakeline Rheinheimer ◽  
Daisy Crispim ◽  
Ana Luiza Maia

ObjectiveThe type 2 deiodinase (D2) is a key enzyme for intracellular triiodothyronine (T3) generation. A single-nucleotide polymorphism in D2 (Thr92Ala) has been associated with increased insulin resistance in nondiabetic and type 2 diabetes (DM2) subjects. Our aim was to evaluate whether the D2 Thr92Ala polymorphism is associated with increased risk for DM2.Design and methodsA case–control study with 1057 DM2 and 516 nondiabetic subjects was performed. All participants underwent genotyping of the D2 Thr92Ala polymorphism. Additionally, systematic review and meta-analysis of the literature for genetic association studies of D2 Thr92Ala polymorphism and DM2 were performed in Medline, Embase, LiLacs, and SciELO, and major meeting databases using the terms ‘rs225014’ odds ratio (OR) ‘thr92ala’ OR ‘T92A’ OR ‘dio2 a/g’.ResultsIn the case–control study, the frequencies of D2 Ala92Ala homozygous were 16.4% (n=173) versus 12.0% (n=62) in DM2 versus controls respectively resulting in an adjusted OR of 1.41 (95% confidence intervals (CI) 1.03–1.94, P=0.03). The literature search identified three studies that analyzed the association of the D2 Thr92Ala polymorphism with DM2, with the following effect estimates: Mentuccia (OR 1.40 (95% CI 0.78–2.51)), Grarup (OR 1.09 (95% CI 0.92–1.29)), and Maia (OR 1.22 (95% CI 0.78–1.92)). The pooled effect of the four studies resulted in an OR 1.18 (95% CI 1.03–1.36, P=0.02).ConclusionsOur results indicate that in a case–control study, the homozygosity for D2 Thr92Ala polymorphism is associated with increased risk for DM2. These results were confirmed by a meta-analysis including 11 033 individuals, and support a role for intracellular T3 concentration in skeletal muscle on DM2 pathogenesis.


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