We found that FP treatment improved heart function, reduced cardiac fibrosis, and downregulated the expression of fibrosis-related factors including collagen I, collagen III, matrix metalloproteinase-2 (MMP-2), MMP-9, transforming growth factor-<i>β</i>1 (TGF-<i>β</i>1), and p-Smad2/3, which coincided with the upregulated expression of silent information regulator 1 (SIRT1) in the hearts of MI rats.
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.
Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction.
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.
These improvements were associated with decreased expression of matrix metalloproteinase 9, the cardiac stress genes for natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide), and β-myosin heavy chain after MI.
Therefore, our results suggest that TAPE may regulate EPC mobilization through up-regulating the expression level of VEGF, eNOS, NO and MMP-9 in the myocardium of AMI rats.
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).
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.
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.
The focus of this review is to summarize findings on biomarkers of myocardial fibrosis (PICP and PIIINP), profibrotic mediators (TGF-beta1), extracellular matrix remodeling (MMP-9), myocardial stretch (BNP and NTpro-BNP), inflammation (interleukins, C-reactive protein and sCD40L), and myocardial necrosis (high-sensitivity troponin T), biomarkers, that can be used in clinical practice to stratify patients at risk for POAF.
The expression of matrix metalloproteinase 2 (MMP-2), MMP-9, collagen type I, α-smooth muscle actin (α-SMA), and transforming growth factor-β (TGF-β) were upregulated in ISO-induced MI in rats.
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).
Systemic MMP9 elevation is independent of the associated myocardial necrosis and systemic inflammation (measured by Troponin I and C-reactive protein, respectively).
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.
Role of proinflammatory alleles in longevity and atherosclerosis: results of studies performed on -1562C/TMMP-9 in centenarians and myocardial infarction patients from Sicily.
Our results showed that ellagic acid significantly reduced protein expression of HDAC1, mRNA expression of collagen I, collagen III, MMP-2 and MMP-9 and the area of cardiac fibrosis in MI rats.
Nicorandil suppresses the increases in plasma level of matrix metalloproteinase activity and attenuates left ventricular remodeling in patients with acute myocardial infarction.