ArticlePhysiological genomics2012
NFE2L2 pathway polymorphisms and lung function decline in chronic obstructive pulmonary disease.
Article in Physiological genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Immune-mediated genetic pathways resulting in pulmonary function impairment increase lung cancer susceptibility.Nature communications · 2020Article
- Expression of Keap1 and Nrf2 in diffuse large B-cell lymphoma and its clinical significance.Experimental and therapeutic medicine · 2018Article
- Lung function decline over 25 years of follow-up among black and white adults in the ARIC study cohort.Respiratory medicine · 2016Article
- Antioxidant response genes sequence variants and BPD susceptibility in VLBW infants.Pediatric research · 2015Article
- NFE2L2 polymorphisms, mortality, and metabolism in the general population.Physiological genomics · 2014Article
- Article
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
An oxidant-antioxidant imbalance in the lung contributes to the development of chronic obstructive pulmonary disease (COPD) that is caused by a complex interaction of genetic and environmental risk factors. Nuclear erythroid 2-related factor 2 (NFE2L2 or NRF2) is a critical molecule in the lung's defense mechanism against oxidants. We investigated whether polymorphisms in the NFE2L2 pathway affected the rate of decline of lung function in smokers from the Lung Health Study (LHS)(n = 547) and in a replication set, the Vlagtwedde-Vlaardingen cohort (n = 533). We selected polymorphisms in NFE2L2 in genes that positively or negatively regulate NFE2L2 transcriptional activity and in genes that are regulated by NFE2L2. Polymorphisms in 11 genes were significantly associated with rate of lung function decline in the LHS. One of these polymorphisms, rs11085735 in the KEAP1 gene, was previously shown to be associated with the level of lung function in the Vlagtwedde-Vlaardingen cohort but not with decline of lung function. Of the 23 associated polymorphisms in the LHS, only rs634534 in the FOSL1 gene showed a significant association in the Vlagtwedde-Vlaardingen cohort with rate of lung function decline, but the direction of the association was not consistent with that in the LHS. In summary, despite finding several nominally significant polymorphisms in the LHS, none of these associations were replicated in the Vlagtwedde-Vlaardingen cohort, indicating lack of effect of polymorphisms in the NFE2L2 pathway on the rate of decline of lung function.
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