Cargando…

Matrix Metalloproteinase-2 Polymorphisms and Incident Coronary Artery Disease: A Meta-Analysis

Previous studies have yielded controversial results related to the contribution of matrix metalloproteinase-2 (MMP-2) -1306 C/T and -735 C/T polymorphisms in the progression of coronary artery disease (CAD). This study aimed to provide strong evidence for the role of the 2 polymorphisms in genetic r...

Descripción completa

Detalles Bibliográficos
Autores principales: Shi, Yujie, Zhang, Jian, Tan, Chen, Xu, Wei, Sun, Qi, Li, Junxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4504545/
https://www.ncbi.nlm.nih.gov/pubmed/26166126
http://dx.doi.org/10.1097/MD.0000000000000824
Descripción
Sumario:Previous studies have yielded controversial results related to the contribution of matrix metalloproteinase-2 (MMP-2) -1306 C/T and -735 C/T polymorphisms in the progression of coronary artery disease (CAD). This study aimed to provide strong evidence for the role of the 2 polymorphisms in genetic risk of CAD. The human case-control studies regarding the association of MMP-2 polymorphisms with CAD risk were systematically identified through online databases (PubMed, Embase, the Cochrane Library, and CNKI) and manual search. Inclusion criteria were defined for the eligible studies. The fixed-effects meta-analysis was performed to combine the values when homogeneity was indicated. Alternatively, the random-effects meta-analysis was utilized. A total of 2118 samples were analyzed in the meta-analysis of -1306 C/T. The odds ratio for the initially tested genetic model was 0.93 (95% confidence interval: 0.78–1.10 under TT + CT vs CC). The remaining comparisons similarly showed -1306 C/T genotypes were not significantly associated with the risk of CAD. We noted the same trend when data were retrained to myocardial infarction studies. Meta-analysis of -735 C/T suggested no clear association with the development of CAD. The results of the current work fail to support a significant involvement of MMP-2 -1306 C/T and -735 C/T polymorphisms in the risk of developing CAD.