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Published on: April 1, 2019
Association between thrombomodulin polymorphisms and coronary artery disease risk: a meta-analysis
Shuai Zhang1, Zhe Zhang2, Feng Zhang2
1Emergency Center, Ji'nan Sixth People's Hospital, Zhangqiu, China (mainland).
Insights
Thrombomodulin (TM) gene variations, specifically -33G/A and Ala455Val, are identified as significant risk factors for coronary artery disease (CAD). This meta-analysis confirms their association with increased CAD susceptibility.
Area of Science:
- Genetics
- Cardiovascular Medicine
- Molecular Biology
Background:
- The relationship between thrombomodulin (TM) gene polymorphisms and coronary artery disease (CAD) risk is debated.
- Previous studies have yielded conflicting results regarding this association.
Purpose of the Study:
- To systematically evaluate the association between thrombomodulin (TM) gene polymorphisms and the risk of developing coronary artery disease (CAD).
- To clarify the controversial findings through a comprehensive meta-analysis.
Main Methods:
- A systematic literature search was conducted across PubMed, EMBASE, and CNKI databases up to February 2014.
- Meta-analysis was employed to assess the association using odds ratios (ORs) and 95% confidence intervals (CIs).
- Fourteen case-control studies comprising 5493 cases and 8297 controls were included.
Main Results:
- A significant association was found between the TM -33G/A polymorphism and an increased risk of CAD (OR=1.61; 95% CI, 1.35-1.92).
- The TM Ala455Val polymorphism also demonstrated a significant association with elevated CAD risk (OR=1.14; 95% CI, 1.05-1.24).
- These findings remained statistically significant after adjusting the ORs.
Conclusions:
- The TM -33G/A and Ala455Val polymorphisms are identified as significant risk factors for coronary artery disease (CAD).
- These genetic variations contribute to CAD susceptibility.
Background:
The associations between the thrombomodulin (TM) polymorphisms and coronary artery disease (CAD) risk remain controversial. The aim of this study was to evaluate the association of TM polymorphisms with CAD susceptibility using a meta-analysis approach.
Material/Methods:
All eligible studies were identified through a search of PubMed, EMBASE, and China National Knowledge Infrastructure (CNKI) before February 2014. The associations between the TM polymorphisms and CAD risk was assessed by odds ratios (ORs) and 95% confidence intervals (CIs).
Results:
A total of 14 case-control studies, including 5493 cases and 8297 controls, were eventually collected. There was a significant association between TM -33G/A polymorphism and CAD risk (OR=1.61; 95% CI, 1.35-1.92; I2=15%). The TM Ala455Val polymorphism was also associated with a significantly increased CAD risk (OR=1.14; 95% CI, 1.05-1.24; I2=0%). These results remained statistically significant when the adjusted ORs were combined.
Conclusions:
Our results suggest that TM-33G/A and Ala455Val polymorphisms are risk factors for CAD.
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