|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Indirect merging PPi demonstrated that the interacting network of TP53, IL8, CCR2, HSPA1A, ELANE, PIK3CA was associated with the development of emphysema.
|
30532529 |
2019 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our previous studies indicated that placenta growth factor (PGF) and PGF-triggered downstream signaling molecules mediate NE-induced lung epithelial cell apoptosis, which is a major pathogenic mechanism for pulmonary emphysema.
|
29722565 |
2018 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although rBmTI-6-D1, did not present a neutrophil elastase (NE) inhibitory activity, the results show that the inhibitor interfered in the pathway of NE secretion in PPE-emphysema mice model.
|
29339284 |
2018 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
This causes a deficiency of the inhibitor of neutrophil elastase, which results in increased degradation of lung elastin and the development of pulmonary emphysema.
|
29461896 |
2018 |
|
Pulmonary Emphysema
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Sputum free neutrophil elastase activity was significantly elevated in the group with emphysema on CT imaging.
|
29247616 |
2018 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alpha-1 antitrypsin (AAT) deficiency-associated emphysema is largely attributed to insufficient inhibition of neutrophil elastase released from neutrophils.
|
28362108 |
2017 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data suggest that type VI collagen turnover and elastin degradation by neutrophil elastase are associated with COPD-induced inflammation (eosinophil-bronchitis) and emphysema.
|
28103932 |
2017 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Proteolytic attack of NE on peripheral organs, more exclusively on lung parenchyma has severe consequence that may precipitate pulmonary emphysema.
|
27492524 |
2016 |
|
Pulmonary Emphysema
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Progressive airway wall remodelling and emphysema in pIgR(-/-) mice are associated with an altered lung microbiome, bacterial invasion of the airway epithelium, NF-κB activation, leukocyte infiltration and increased expression of matrix metalloproteinase-12 and neutrophil elastase.
|
27046438 |
2016 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although neutrophil elastase is implicated in the pathophysiology of emphysema, our results highlight a potentially important role for proteinase 3 because of its greater concentration in azurophil granules, its reduced association rate constant with all α-1-antitrypsin variants studied here, its greater diffusion distance, time spent uninhibited following degranulation, and its greater propensity to partition to α-2-macroglobulin where it retains proteolytic activity.
|
25416382 |
2015 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inheritance of the F variant of alpha-1-antitrypsin is associated with normal circulating protein levels, but it is believed to be dysfunctional in its ability to inhibit neutrophil elastase and therefore has been implicated as a susceptibility factor for the development of emphysema.
|
25098359 |
2014 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study hypothesized that excessive NE may up-regulate PlGF and that PlGF-induced LE apoptosis mediates the pathogenesis of pulmonary emphysema.
|
25186164 |
2014 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
The rationale of α1-antitrypsin (AAT) augmentation therapy to treat progressive emphysema in AAT-deficient patients is based on inhibition of neutrophil elastase; however, the benefit of this treatment remains unclear.
|
23975926 |
2013 |
|
Pulmonary Emphysema
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Alpha-1-antitrypsin (A1AT) is the main inhibitor of neutrophil elastase, and severe alpha-1-antitrypsin deficiency (A1ATD) is a genetic risk factor for early-onset emphysema.
|
22971141 |
2012 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Imbalance between neutrophil elastase and alpha-1-antitrypsin (AAT) leads to emphysema in smokers as well as in patients with inherited alpha-1-antitrypsin deficiency.
|
20521180 |
2011 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Severe AAT deficiency (plasma levels below 11 μm) is most commonly associated with an adult-onset lung disease, with pan-acinar emphysema and airway inflammation, which is thought to be primarily owing to the loss of function of AAT in neutralizing neutrophil elastase and other pro-inflammatory enzymes.
|
21498872 |
2011 |
|
Pulmonary Emphysema
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Excessive neutrophil elastase (NE) activity and altered vascular endothelial growth factor (VEGF) signaling have independently been implicated in the development and progression of pulmonary emphysema.
|
19136576 |
2009 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, NE could be considered to have potential multiple roles in the pathogenesis of both emphysema and lung fibrosis.
|
18243764 |
2008 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Its major physiological role is inhibition of neutrophil elastase in the lungs, and its deficiency is associated with progressive ultimately fatal emphysema.
|
16773239 |
2006 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Emphysema is thought to be caused by the lack of circulating alpha1-AT to inhibit neutrophil elastase in the lung.
|
10677536 |
2000 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
The prime functions of alpha 1AT is to inhibit neutrophil elastase, and a proportion of individuals who are deficient in alpha 1AT develop emphysema.
|
9158819 |
1997 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alpha 1-antitrypsin (AAT) deficiency is a genetic disease in which low serum and lung levels of the antiprotease AAT cause a deficiency of the anti-elastase defensive screen of the lower respiratory tract such that neutrophil elastase is free to degrade the connective tissue of the lung, eventually resulting in emphysema.
|
2117165 |
1990 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
The importance of the destructive element in emphysema and the gradual focusing on neutrophil elastase as a key enzyme in the pathogenesis of emphysema in alpha 1-antitrypsin deficiency is emphasized.
|
2117160 |
1990 |
|
Pulmonary Emphysema
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, for the alpha 1AT protein that does reach the circulation, this mutation markedly affects the ability of the molecule to inhibit neutrophil elastase; i.e., the alpha 1AT Mmineral springs allele predisposes to emphysema on the basis of serum apha 1AT deficiency coupled with alpha AT dysfunction.
|
1967187 |
1990 |
|
Pulmonary Emphysema
|
0.100 |
Biomarker
|
disease |
BEFREE |
The emphysema associated with the inherited serum deficiency of alpha 1-antitrypsin appears to result from an imbalance between neutrophil elastase and its major inhibitor within the alveolar structures.
|
7028785 |
1981 |