Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
This novel ELISA will be useful for further clarifying the impact of EL on HDL metabolism and atherosclerosis.
|
31473149 |
2019 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of EL has been shown to increase HDL concentration in preclinical animal models and was targeted as a potential treatment of atherosclerosis.
|
30613337 |
2018 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus far, the extensive investigations of LIPG have focused on its mechanisms and involvement in metabolic syndromes such as atherosclerosis.
|
28540715 |
2018 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Endothelial lipase (EL) reportedly reduces HDL levels, which, in theory, would increase atherosclerosis.
|
29748333 |
2018 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Increased hepatic expression of EL attenuates cholesterol diet-induced hypercholesterolemia and protects against atherosclerosis.
|
28546217 |
2017 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
To investigate the effects of inflammatory factor interleukin (IL)‑6 on the expression of endothelial lipase (EL) and its potential signaling pathways in atherosclerosis, a primary culture of human umbilical vein endothelial cells (HUVECs) was established and treated as follows: i) Control group without any treatment; ii) recombinant human (rh)IL‑6 treatment (10 ng/ml) for 0, 4, 8, 12 and 24 h; iii) p38 mitogen‑activated protein kinases (MAPKs) inhibitor (SB203580, 10 µmol/l) pretreatment for 1 h prior to rhIL‑6 (10 ng/ml) treatment; iv) nuclear factor (NF)‑κB activation inhibitor (pyrrolidine dithiocarbamate, 10 mmol/l) pretreatment for 1 h prior to rhIL‑6 (10 ng/ml) treatment.
|
27430252 |
2016 |
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The purpose of our study was to investigate the effects of endothelial lipase gene polymorphism and inflammation markers (CRP, IL-1β, IL-6, IL-8 and TNF-α) in the atherosclerosis.
|
23673478 |
2013 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although a small number of mutations in LIPG have been described, the role of LIPG in protection against atherosclerosis is unclear.
|
23243195 |
2013 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
rEL is expressed in multiple tissues and may have many physiological and pathophysiological functions, such as in the regulation of cholesterol metabolism and atherosclerosis.
|
22240910 |
2012 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, in atherosclerosis prone LDLR(-/-)ApoB(100/100) mice, systemic adenoviral gene transfer with human VEGF-A decreased EL mRNA in peripheral tissues and increased plasma HDL cholesterol.
|
23102786 |
2012 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
More mechanistic insights into the diverse biological properties of these enzymes are therefore required to firmly establish EL and HL as targets for the treatment of atherosclerotic cardiovascular disease.
|
21424685 |
2011 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, we believe that endothelial lipase might be a promising marker for atherosclerosis in clinical settings in the future.
|
20621031 |
2010 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The available data regarding the impact of EL expression and activity on HDL metabolism, reverse cholesterol transport, and atherosclerosis are reviewed.
|
20962428 |
2010 |
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We hypothesized that EL concentrations would be associated with decreased HDL-C and increased atherosclerosis in humans.
|
16354105 |
2006 |
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Unlike LPL and HL, EL is located in the vascular endothelial cells and its expression is highly regulated by cytokines and physical forces, suggesting that it may play a role in the development of atherosclerosis.
|
12401876 |
2002 |