Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.35 (matrix metalloproteinase 9)
 2,207 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Matrix metalloproteinases contribute to vascular remodeling by breaking down extracellular-matrix while new matrix is synthesized. Of the variety of MMPs, stromelysin-1 and gelatinase B may have key roles in coronary artery atherosclerosis. Moreover, The 5A/6A polymorphism in the promoter region of the stromelysin-1 gene may be a pathogenetic risk factor for acute myocardial infarction. Gelatinase B (92-kDa type IV collagenase and MMP-9) is one of the MMPs found to be highly expressed in the disruption-prone regions of atherosclerotic plaques. C- to T substitution at the promoter site (-1562) resulted in the higher promoter activity of the T-allelic promoter. The R279Q polymorphism in exon 6 led to the substitution of adenosine by guanine, and was a common polymorphism in the general population. We evaluated the relation between these polymorphisms and stable angina, the severity of atherosclerosis in coronary artery disease, and in-stent restenosis after percutaneous coronary angioplasty. The study population was composed of 131 patients with stable angina (mean age 61.3 years, 89 males) and 117 control subjects (mean age 59.3 years, 59 males). Coronary angiographies were performed in all cases at Yonsei University Cardiovascular Hospital from February 1998 to June 2000. The genotype for each polymorphism was determined using a SNaPshotTM kit and by restriction fragment length polymorphism (RFLP). The prevalence of 5A containing a polymorphism of the stromelysin-1 gene was higher in the stable angina group than in control patients, but no difference in the two polymorphisms of the gelatinase B gene was found between the two groups. By multiple logistic analysis, the 5A-allele of the stromelysin-1 gene was found to be an independent risk factor of stable angina with an odds ratio of 2.29 (95% CI; 1.19-4.38). However, the severity of atherosclerosis in coronary artery or in stent restenosis was not related to any polymorphism of stromelysin-1 or gelatinase B. Our results show that functional genetic variation of stromelysin-1 could be a significant risk factor for stable angina, and might play an important role in coronary atherosclerosis involving vascular remodeling.
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PMID:The roles of stromelysin-1 and the gelatinase B gene polymorphism in stable angina. 1220 36

We measured levels of matrix metalloproteinase 9 (MMP-9) as a potential risk factor in 75 patients with acute coronary syndrome (ACS) compared to 25 patients with stable angina (SA) and 20 healthy participants. Patients were studied stressing on smoking, hypertension, diabetes, lipid profile, cardiac enzymes, MMP-9, and electrocardiography. Patients with ACS had higher MMP-9 levels than the SA group. The highest MMP-9 levels were found among ST-elevated myocardial infarction (MI), while the lowest levels were found among the control group. The MMP-9 level was significantly higher among patients with ACS having poor disease outcome (recurrent ischemic attacks, congestive heart failure, or death). The MMP-9 cutoff value of 3100 pg/mL was able to discriminate MI from unstable angina (UA), while the best prognostic utility was established at 4700 pg/mL. We suggest that serum MMP-9 could be an early marker that discriminates MI from UA and predicts poor outcome in terms of disease severity and extent of disease complications.
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PMID:Clinical Relevance of matrix metalloproteinase 9 in patients with acute coronary syndrome. 2561 88