Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Significant increased activation of TNF-α, Caspase-3 activity and myocardial infarct size in DOX-treated group.
|
31630586 |
2019 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
We showed that punicalagin-treated group exhibited enhanced cardiac function, reduced myocardial infarction and decreased cleaved caspase-3 level.
|
31063767 |
2019 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
At the same time, NPY-knockout rats exhibited a remarkable decrease in infarct size, serum lactate dehydrogenase activity, cardiomyocyte apoptosis, and caspase-3 expression and activity and a strong improvement in heart contractile function compared with MI rats.
|
31708788 |
2019 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
It was found that after miR-34a antagomir reversed FS (%) and EF (%) in MI rats, the messenger RNA (mRNA) and protein levels of Caspase-3 in Sham group and MI + miR-34a antagomir group were significantly lower than those in the MI group (p < 0.05), indicating that the addition of miR-34a antagomir inhibited myocardial cell apoptosis after infarction, while the mRNA and protein levels of Wnt/β-catenin were both higher than those in the MI group.
|
30964183 |
2019 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Transplantation of cardiac Sca-1-positive cells rather than c-Kit-positive cells preserves mitochondrial oxygen consumption of the viable myocardium following myocardial infarction in rats.
|
31375326 |
2019 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Also, terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling staining and the expression of cleaved caspase 3 suggested that MI-induced myocytes apotosis was inhibited by PTHrP 87 to 139.
|
30994964 |
2019 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Furthermore, reconstitution of Sca-1 KO mice with WT Sca-1<sup>+</sup> cells was associated with the reactivation of EMT and improved cardiac function after MI.
|
29556355 |
2018 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Caspase-3 activity was higher in the amygdala (medial and lateral) and hippocampal CA3 region in untreated MI rats, whereas caspase-6 activity was higher in the CA1 region.
|
30486235 |
2018 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
<i>In vivo</i>, the MI mice exhibited worse cardiac function by echocardiographic assessment and showed larger myocardial scarring by light microscopy, whereas aliskiren treatment reversed these effects, which were also associated with the changes in caspase-3 and Bcl-2 expression as well as in the number of apoptotic cells.
|
29184499 |
2017 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
MicroRNA-98 negatively regulates myocardial infarction-induced apoptosis by down-regulating Fas and caspase-3.
|
28784995 |
2017 |
Myocardial Infarction
|
0.600 |
Therapeutic
|
disease |
RGD |
Ad-HGF improves the cardiac remodeling of rat following myocardial infarction by upregulating autophagy and necroptosis and inhibiting apoptosis.
|
27904666 |
2016 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
CTD_human |
Attenuation of ER stress prevents post-infarction-induced cardiac rupture and remodeling by modulating both cardiac apoptosis and fibrosis.
|
25450231 |
2015 |
Myocardial Infarction
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Erythropoietin administration after myocardial infarction reduced caspase 3 expression (apoptotic activity) and induced neovascularization around the infarct area.
|
23453036 |
2013 |
Myocardial Infarction
|
0.600 |
Biomarker
|
disease |
BEFREE |
Kallikrein gene delivery improved cell survival parameters as shown by increased phospho-Akt and reduced caspase-3 activation at 2 weeks after MI.
|
12411458 |
2002 |