NFE2L2, nuclear factor, erythroid 2 like 2, 4780

N. diseases: 823; N. variants: 34
Disease: Chronic Obstructive Airway Disease ×
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 Biomarker disease RGD The levels of KLF2, gamma-GCS mRNA were markedly increased in the COPD group (all P < 0.01) while Nrf2 mRNA expression in COPD group had no significant difference with that in control group ( P > 0.05). 22737924 2012
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 AlteredExpression disease BEFREE The transcription factor NRF2 is a critical player in the battle against oxidative stress and its function is impaired in COPD. 27832175 2016
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 Biomarker disease BEFREE Therapy with astaxanthin directed toward activating the Nrf2 pathway has the potential to be a novel preventive and therapeutic strategy for COPD. 31795292 2019
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 Biomarker disease BEFREE Therefore we studied the relation between NFE2L2 and all-cause, cardiovascular, and COPD mortality and its associations with triglyceride and cholesterol levels. 24790085 2014
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 AlteredExpression disease BEFREE Therefore, PI3K/Akt pathway may play an important role in the activation of Nrf2 and COPD inflammation. 30827233 2019
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 Biomarker disease BEFREE This data-mining review supports the notion that Nrf2-regulated anti-oxidant genes play a central role in protection against tobacco smoke toxic effects and may be amenable to use as COPD risk biomarkers. 20594977 2010
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 GeneticVariation disease BEFREE To date, researchers have discovered that Nrf2 deletion results in high susceptibility and severity of insults in various models of respiratory diseases, including bronchopulmonary dysplasia (BPD), respiratory infections, acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, idiopathic pulmonary fibrosis (IPF), and lung cancer. 30728889 2019
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 AlteredExpression disease BEFREE Under disease conditions, PSTC engaged its target, inducing the expression of Nrf2-regulated genes in human bronchial epithelial cells derived from patients with chronic obstructive pulmonary disease, as well as in the lungs of cigarette smoke-exposed mice. 28790194 2017
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 AlteredExpression disease BEFREE We also demonstrated that expression of the Nrf2-regulated antioxidant enzymes was decreased in a patient with chronic obstructive pulmonary disease associated with PH. 23590302 2013
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 Biomarker disease BEFREE We conclude that NRF2 is a novel drug target for reversing corticosteroid resistance in COPD and other corticosteroid-resistant inflammatory diseases. 22005302 2011
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 Biomarker disease BEFREE We identified that VCP also mediates proteasomal degradation of HDAC2 and Nrf2, as a potential mechanism for increased oxidative stress and corticosteroid resistance in COPD subjects with emphysema. 21318260 2011
CUI: C0024117
Disease: Chronic Obstructive Airway Disease
Chronic Obstructive Airway Disease 		0.300 AlteredExpression disease BEFREE We verified using the preclinical COPD-emphysema murine model that chronic CS (Ch-CS)-induced inflammation (interleukin [IL]-6/IL-1β levels), aggresome formation (perinuclear coexpression/colocalization of ubiquitinated proteins [Ub] and p62 [impaired autophagy marker], and CFTR), oxidative/nitrosative stress (p-Nrf2, inducible nitric oxide synthase [iNOS], and 3-nitrotyrosine expression), apoptosis (caspase-3/7 activity), and alveolar airspace enlargement (Lm) are significantly (p < 0.05) alleviated by augmenting airway GSNO levels. 28006950 2017