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Association of tumor necrosis factor-α -308 G/A gene polymorphism with coronary artery diseases: An evidence-based
Elaheh Kazemi1,2, Khadijeh Jamialahmadi3,4, Amir Avan5
1Department of Biochemistry, International Campus of Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Insights
The Tumor necrosis factor-alpha (TNF-α) 308G/A gene variant is linked to coronary artery disease (CAD) risk. Specifically, the AA genotype is associated with increased CAD risk and higher C-reactive protein levels.
Area of Science:
- Genetics
- Cardiology
- Molecular Biology
Background:
- Coronary artery disease (CAD) is a leading global cause of mortality.
- Identifying molecular markers for CAD risk is crucial.
- Tumor necrosis factor-alpha (TNF-α) plays a significant role in CAD development.
Purpose of the Study:
- To investigate the association between the TNF-α 308 (G/A) gene polymorphism and CAD.
- To determine if this polymorphism correlates with disease severity and biochemical markers.
Main Methods:
- Analyzed TNF-α 308 gene polymorphism in 903 individuals (222 controls, 681 CAD patients).
- Assessed CAD severity via angiography (≥50% vs. <50% stenosis).
- Evaluated biochemical profiles including lipids, glucose, and C-reactive protein (CRP).
Main Results:
- TNF-α-AA or AG genotypes were less frequent in CAD patients compared to controls.
- The TNF-α-308-AA genotype showed a 3.56-fold increased risk of CAD (≥50% stenosis).
- This genotype was also associated with higher blood pressure and CRP levels in CAD patients.
Conclusions:
- The TNF-α-308G/A polymorphism is associated with obstructive CAD.
- Further research is warranted to explore the link between this polymorphism and hypertension.
Background:
Coronary artery disease (CAD) is the leading cause of death worldwide and remains a major health problem, providing the rationale for identification of molecular markers for detection of individuals at high risk of developing CAD. Tumor necrosis factor-α (TNF-α) plays a crucial role in the pathogenesis of CAD. We have therefore explored the association of TNF-α 308 (G/A) gene polymorphism in 903 individuals with/without CAD.
Methods:
TNF-α 308 gene polymorphism was analyzed in 903 subjects of whom 222 were healthy controls. Among the 681 patients who were investigated angiographically, 468 had ≧50% stenosis and 213 patients had <50% stenosis. Biochemical profiles (eg, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, fasting blood glucose, and CRP) were evaluated. Associations between TNF-α genotypes with biochemical and anthropometric characteristics were determined.
Results:
The frequencies of TNF-α-AA or AG genotypes were significantly lower in patients classified as CAD patients with ≥ or <50% obstruction in at least one coronary artery, compared to the control group. We observed that CAD patients with ≥50% stenosis and with AA genotype were associated with higher risk of CAD with OR of 3.56 (95%CI: 1.02-12.41; P=.046) using multivariate analysis. Moreover, we found that TNF-α-308-AA genotype was associated with blood pressure and CRP level in CAD patients, compared to the wild type-genotype.
Conclusion:
Our data showed an association of TNF-α-308G/A polymorphism with CAD patients with ≥50% obstruction, supporting the need for further investigations on the role of TNF-α-308G/A polymorphism with hypertension.
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