Role of proinflammatory alleles in longevity and atherosclerosis: results of studies performed on -1562C/TMMP-9 in centenarians and myocardial infarction patients from Sicily.
Bone marrow mesenchymal stem cell transplantation combined with perindopril treatment attenuates infarction remodelling in a rat model of acute myocardial infarction.
Nicorandil suppresses the increases in plasma level of matrix metalloproteinase activity and attenuates left ventricular remodeling in patients with acute myocardial infarction.
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).
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.
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.
Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-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.
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).
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.
Increased expression of α-smooth muscle actin and collagen I/III was observed, whereas the levels of matrix metalloproteinase-2 and matrix metalloproteinase-9 were decreased in the hearts of Dectin-2 knockout mice after MI.
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.