{{Rsnum
|rsid=3025058
|Gene=MMP3
|Chromosome=11
|position=102845217
|Orientation=plus
|GMAF=0.2622
|Gene_s=MMP3
|Assembly=GRCh38
|GenomeBuild=38.1
|dbSNPBuild=141
|geno1=(-;-)
|geno2=(-;T)
|geno3=(T;T)
}}SNP [[rs3025058]] was first described in 1995 as a variant upstream of, and influencing the regulation of, the [[MMP3]] gene. Most commonly, the version of this SNP with a run of 5 A's is called the 5A allele, and an allele with 6 A's is called 6A. Thus, the homozygous genotypes are either 5A/5A or 6A/6A, and the heterozygote genotype is published as 5A/6A. Incidentally, the [[MMP3]] gene is also called stromelysin-1, and although there is a SNP in dbSNP in the orientation that shows the polynucleotide run as A's ([[rs35068180]]) the entry that has population frequency data is the one discussed here, [[rs3025058]], which is from the other strand and thus shows the string as T's.

There have been numerous studies in the last 10+ years linking either the 5A or 6A allele to risk for [[myocardial infarction]] or [[coronary artery disease]]. A relatively recent meta-analysis combining seven previously published studies concluded that the 5A allele is indeed a plaque-disrupting risk factor (odds ratio 1.26, CI: 1.1 - 1.4, p<0.001), while the 6A allele is associated with greater progression of coronary atherosclerosis and the 6A/6A genotype is associated with a worse progression of [[coronary artery disease]] after angioplasty. However, all these studies show a lot of heterogeneity, and gender, age, and ethnicity are all likely to alter the influence of these alleles. {{PMID|16905683|OA=1
}}

{{PMID|19263529|OA=1
}} [[rs1799864]](G), [[rs3025058]](A) and [[rs662]] were associated with increased risk, and [[rs1800775]](A) with reduced risk of recurrent [[venous thromboembolism]]

{{ neighbor
| rsid = 35068180
| distance = 5
}}

{{PMID|19508478}} no influence on varicose veins
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}}

{{on chip | 23andMe v2}}
{{on chip | 23andMe v3}}
{{on chip | 23andMe v4}}