Key result
MMP3 Glu45Lys polymorphism linked to ~52% higher CAD risk.
Why the study?
Are matrix metalloproteinase (MMP) family gene polymorphisms associated with an increased risk for coronary artery disease?
Meta-Analysis
Are matrix metalloproteinase (MMP) family gene polymorphisms associated with an increased risk for coronary artery disease?
Odds Ratio: 1.52 (95% CI 1.3–1.76)
p-value: p=<0.001
Polymorphisms in the MMP3 (Glu45Lys) and MMP9 (-1562C/T) genes are significantly associated with an increased susceptibility to coronary artery disease.
MMP3/MMP9 variants may refine CAD susceptibility models; extends candidate-gene data but should not yet change practice.
CONTEXT AND OBJECTIVE: The association between matrix metalloproteinase (MMP) family gene polymorphisms and coronary artery disease (CAD) has been widely evaluated; however, the studies have yielded contradictory results. The authors sought to investigate this inconsistency by performing a comprehensive meta-analysis on MMP family genes. DATA SOURCES: Articles were identified by searches of PubMed, HuGE Navigator, EMBASE, Wanfang, and China Biological Medicine databases before January 2012, and by hand searches of bibliographies of retrieved articles and reviews. STUDY SELECTION: Qualified articles were retrospective or nested case-control studies of MMP family gene polymorphisms and CAD. A total of 11 polymorphisms from five MMP family genes were meta-analysed. Forty-eight articles encompassing 59 studies fulfilled the predefined criteria. DATA EXTRACTION: Data were independently extracted from qualified articles by two reviewers using a standardized Excel template and were verified. Any disagreement was adjudicated by discussion and a consensus was reached. RESULTS: Overall significant associations were observed for Glu45Lys in MMP3 gene under both allelic (OR: 1.52; 95% CI 1.3 to 1.76; p<0.001) and dominant (1.37; 1.23 to 1.54; <0.001) models, and for -1562C/T in MMP9 gene under allelic model (1.11; 1.02 to 1.2; 0.012). Subgroup analyses demonstrated that sources of study heterogeneity stemmed from the CAD endpoint for -519A/G, -1612 6A/5A, Glu45Lys, from the descent of study populations for -1607GG/G, -1612 6A/5A, -790T/G, -1562C/T, from the study design for -1607GG/G, -1612 6A/5A, -1562C/T, and from the selection of controls for -1306C/T, -1562C/T, Arg279Gln. In meta-regression analyses, effect of -1612 6A/5A on CAD was ethnicity-specific (coefficient: 0.21; p=0.048), and this effect was more prominent for myocardial infarction patients or East Asians. CONCLUSIONS: The results provided strong evidence regarding the susceptibility of MMP3 and MMP9 genes to the development of CAD. Future studies incorporating gene-gene and gene-environment interactions are encouraged.
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Niu et al. (2012) conducted a meta-analysis in coronary artery disease. MMP family gene polymorphisms (MMP3 Glu45Lys and MMP9 -1562C/T) vs. Wild-type or absence of polymorphism was evaluated on coronary artery disease (OR 1.52, 95% CI 1.3 to 1.76, p=<0.001). The MMP3 Glu45Lys polymorphism was significantly associated with an increased risk of coronary artery disease under an allelic model (OR 1.52; 95% CI 1.3 to 1.76; p<0.001).
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