Bone marrow mesenchymal stem cell transplantation combined with perindopril treatment attenuates infarction remodelling in a rat model of acute myocardial infarction.
Role of proinflammatory alleles in longevity and atherosclerosis: results of studies performed on -1562C/TMMP-9 in centenarians and myocardial infarction patients from Sicily.
There was a significantly higher incidence of th-1562C>T MMP-9 polymorphism in the AMI patients compared to the control group (27.6% vs 17.9%, p=0.04).
Nicorandil suppresses the increases in plasma level of matrix metalloproteinase activity and attenuates left ventricular remodeling in patients with acute myocardial infarction.
The carriers of this allele have high levels of MMP-9 activity, LDL-C, TC and homocysteine (P=0.01), thus, are more likely to develop myocardial infarction and CAD at young age (less than 55 years).
We aimed to investigate the association between the interaction of 2 single-nucleotide polymorphisms ([SNPs] -1562C>T and R279Q) of the MMP-9 gene and smoking with MI in a Uighur population of China.
The present study suggests that donepezil inhibits the MMP-9-related acute inflammatory tissue injury in the infarcted myocardium, thereby reduces the risk of left ventricular free wall rupture during the acute phase of MI.
This meta-analysis demonstrated that the MMP-3 5A/6A and MMP-9-1562 C→T polymorphisms are risk factors associated with increased MI susceptibility, but these associations vary in different ethnic populations.
Higher MMP-9 gene-expression and TIMP-1 levels were observed in patients with previous myocardial infarction, the latter also was elevated in diabetics (<0.05, all).
Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction.
Significantly higher levels of MMP-2 (299.47 ± 117.61 ng/ml) and MMP-9 (93.56 ± 53.74 ng/ml) were determined in patients with myocardial infarction compared to the controls, in both cases P < 0.001.
Here, we investigated whether expression of MMP-9 and its inhibitors in blood mononuclear cells and plasma were related to depressive symptoms in patients with a recent myocardial infarction (MI).
Global MMP-9 deletion in mouse MI models has proven beneficial, suggesting inhibition of some aspects of MMP-9 activity may be valuable for clinical use.
Furthermore, multiple logistic regression analysis indicated that the individuals with the TT genotype of the MMP-9-1562C>T polymorphism were significantly protected against MI in comparison with the CC genotype (OR: 0.01, 95% CI: 0.002-0.68, p = 0.03).
The TT variants of -1562C/TMMP-9 and at least one T allele of +92C/T MMP-13 were considered in a trend to affect disease progression and long-term survival after myocardial infarction.