|
Pulmonary Fibrosis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
This study is the first to demonstrate that PERK activation contributes to pulmonary fibroblast differentiation elicited by ET-1 or thrombin, and the inhibitory activity of CUR against PF is demonstrated herein.
|
30825198 |
2019 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
We addressed the role of highly selective ET-1 receptor A (ETA) inhibition in the pathogenesis of experimental pulmonary fibrosis by bleomycin (BLM).
|
29131071 |
2018 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Transient Blockade of Endothelin-1 Mitigates Amiodarone-Induced Pulmonary Fibrosis.
|
29516177 |
2018 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Given that endothelial cells are the main source of ET-1 and ET-1 from other cells may encounter difficulty penetrating vascular compartments, we hypothesize that endothelial-derived ET-1 promotes vascular remodeling secondary to pulmonary fibrosis.
|
29947539 |
2018 |
|
Pulmonary Fibrosis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Our studies provide a potential therapeutic approach whereby fenofibrate-induced miR-301a/miR-454 expression can ameliorate PH and lung fibrosis by reduction in ET-1 and PAI-1 levels in SCD.
|
26460070 |
2015 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Endothelin-1 (ET-1) has been shown to be involved in human pulmonary fibrosis.
|
23306833 |
2013 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
The inhibition of FAK with the compound PF-562,271 prevented ET-1-mediated collagen deposition and myofibroblast formation, thereby preventing the development of lung fibrosis.
|
22962065 |
2012 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
This suggests a biologic rationale for the blockade of EDN1 to limit the evolution of lung fibrosis in humans.
|
20055532 |
2010 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
CTD_human |
We also observed significant decreases in pulmonary fibrosis in Group PZ compared with Group P. These findings suggest that GTE inhibits paraquat-induced pulmonary fibrosis by suppression of oxidative stress and ET-1 expression.
|
17235729 |
2007 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
LHGDN |
As elevated JNK activation in fibrotic lung fibroblasts contributes to the persistence of the myofibroblast phenotype in pulmonary fibrosis by promoting an autocrine ET-1 loop, targeting the ETA and ETB receptors or constitutive JNK activation by fibrotic lung fibroblasts is likely to be of benefit in combating chronic pulmonary fibrosis.
|
16809784 |
2006 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Thus, blocking ET-1 or the PI3-kinase/Akt cascades might be beneficial in reducing scar formation in pulmonary fibrosis.
|
15047866 |
2004 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
LHGDN |
Our results suggest that ET-1 induces a program of matrix synthesis in lung fibroblasts and that ET-1 may play a key role in connective tissue deposition during wound repair and in pulmonary fibrosis.
|
15044479 |
2004 |
|
Pulmonary Fibrosis
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Percutaneous injection of the plasmid containing the human endothelin-1 (hET-1) gene driven by a CMV promoter (pRc/CMVhET-1) in combination with cationic lipids into the lungs caused pulmonary fibrosis localized to the injection site in the peripheral lungs.
|
11000124 |
2000 |
|
Pulmonary Fibrosis
|
0.600 |
Biomarker
|
disease |
RGD |
To determine the role of ET-1 and endothelin-converting enzyme (ECE)-1 and the effect of Bosentan, an ET receptor antagonist, in an animal model of IPF, we studied three groups of rats (n = 6 each): Group 1, control, received saline; Group 2, fibrosis, received 1.5 U bleomycin intratracheally; Group 3, fibrosis-Bosentan treated, received bleomycin and Bosentan daily by gavage.
|
9279246 |
1997 |