Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
The injection of CBD-VEGF improved cardiac function in rats with induced acute myocardial infarction.
|
19307480 |
2009 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study is designed to clarify the regulatory mechanisms underlying VEGF-A, ROS, ER stress, autophagy, and angiogenesis in acute myocardial infarction (AMI).
|
30793306 |
2019 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study demonstrates that PF hydrogels can simultaneously provide mechanical support to attenuate adverse myocardial remodelling, and a pro-angiogenic benefit from the sustained VEGF and ANG1 delivery that culminates in a restorative effect following MI.
|
27756647 |
2017 |
Acute myocardial infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our data indicate that the -634 polymorphism and its co-inheritance with genotypes of other VEGF polymorphisms might be considered as risk factors playing a role in the clinical outcome of AMI patients.
|
19332989 |
2009 |
Acute myocardial infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the connectivity map generated by AutoCM a group of variables was directly linked with the AMI status; these were: gender (male), early age at onset (50-65 years), HMGCR gene (CC wild type genotype), IL-1betaCT, IL-6 GG and VEGF CC genotypes.
|
20388088 |
2010 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
CONCLUSIONS miR-126 and rosuvastatin have protective effects on AMI risk, and VEGF-A antagonizes effects on AMI is imposed by.
|
27376405 |
2016 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
We hypothesized that transplantation of VEGF-expressing MSCs could effectively treat acute myocardial infarction (MI) by providing enhanced cardioprotection, followed by angiogenic effects in salvaging ischemic myocardium.
|
15831811 |
2005 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We demonstrated that ADTM (12-24 mg/kg) treatment for 14 days significantly decreased myocardial infarct size, increased the blood vessel density compared to vehicle in the myocardial peri-infarct area, and ADTM (24 mg/kg) enhanced the serum VEGF level in MI mice (P < 0.05).
|
29890255 |
2018 |
Acute myocardial infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Changes of soluble CD40 ligand in the progression of acute myocardial infarction associate to endothelial nitric oxide synthase polymorphisms and vascular endothelial growth factor but not to platelet CD62P expression.
|
26279254 |
2015 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study investigated the time course of TB4 and VEGF during AMI, cardiac arrest, and resuscitation.
|
21332365 |
2011 |
Acute myocardial infarction
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Variation in the VEGF gene is weakly associated with IMT and the risk of AMI, but the effect can only be observed when the information of the SNPs is combined by constructing haplotypes.
|
19089753 |
2009 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
Specifically, among SCD cases, increased MYL3, VEGFA and MMP9 values in the anterior wall of the right ventricle were found when the confirmed cause of death was acute myocardial infarction (AMI).
|
31419595 |
2019 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
In large mammalian models of acute myocardial infarction (AMI), plasmid-mediated vascular endothelial growth factor (pVEGF) gene transfer has been shown to induce angio-arteriogenesis, proliferation of myocyte precursors and adult cardiomyocyte mitosis, reducing infarct size at 15 days after coronary artery occlusion.
|
21954009 |
2012 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, HSYA increased the mRNA expressions of VEGF-A and MMP-9 in the extract of antinucleolin antibody-precipitated protein from the heart of AMI mice.
|
29512890 |
2018 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Western blot analysis indicated that VEGF and SDF‑1α were upregulated in resveratrol‑treated myocardium after a 7 day treatment or 4 weeks after AMI (7 days VEGF PBS vs. Res, 0.89±0.07 vs. 1.21±0.02, P<0.05; SDF‑1α PBS vs. Res, 0.66±0.04 vs. 1.33±0.04, P<0.05; 4 weeks VEGF CSCs vs. Res + CSCs, 0.54±0.03 vs. 0.93±0.13, P<0.05; SDF‑1α CSCs vs. Res + CSCs, 0.53±0.03 vs. 0.93±0.03, P<0.05).
|
28138705 |
2017 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
Compared with AMI group and AMI + E group, in the AMI + PLV-PI3KCG group, left ventricular end diastolic diameter (LVEDd) was decreased, left ventricular ejection fraction (LVEF%) was significantly increased, and vascular endothelial growth factor (VEGF) expression was significantly increased in the infarct region (P<0.05); PI3KCG, pAkt/Akt, HIF-1a, and Bcl-2/Bax protein expressions were significantly increased (P<0.05).
|
29607167 |
2018 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Compared with the AMI group, BHD promoted the expression of Cav-1, VEGF, VEGFR2, and p-ERK in the infarction border zone after AMI.
|
31178960 |
2019 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Transplantation of MNCs expressing hVEGF increased the wall thickness of the scar in the heart after AMI.
|
19167769 |
2010 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
Finally, we considered insulin-like growth factor 1 receptor and vascular endothelial growth factor A as two candidate drug targets by utilizing the cardiac hypertrophy and AMI pathways.
|
30514363 |
2018 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We found that, compared with the AMI model rats, in rats treated by TPAE, the CEPC counts, the expression of VEGF, eNOS, NO, and MMP-9 in myocardial tissue and their plasma content all increased more rapidly 7 days after AMI and remained at higher level (<i>P</i> < 0.05 or <i>P</i> < 0.01).
|
29387016 |
2017 |
Acute myocardial infarction
|
0.100 |
Biomarker
|
disease |
BEFREE |
We hypothesized that transplantation of VEGF-expressing myoblasts could effectively treat acute myocardial infarction by providing VEGF-induced cardioprotection through vasodilatation in the early phase, followed by angiogenesis effects in salvaging ischemic host myocardium combined with the functional benefits of newly formed, skeletal myoblast-derived muscle in the later phase.
|
11568057 |
2001 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, the increased vascular endothelial growth factor expression could play an essential role in cardiac repair following the onset of acute myocardial infarction.
|
29462681 |
2018 |
Acute myocardial infarction
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Vascular endothelial growth factor mRNA synthesis by peripheral blood mononuclear cells in patients with acute myocardial infarction.
|
11690665 |
2001 |