ArticleExperimental lung research2015
Polymorphisms in key pulmonary inflammatory pathways and the development of acute respiratory distress syndrome.
Article in Experimental lung research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Personalized medicine using omics approaches in acute respiratory distress syndrome to identify biological phenotypes.Respiratory research · 2022Review
- Genetic variation in CSF2 (5q31.1) is associated with longitudinal susceptibility to pediatric malaria, severe malarial anemia, and all-cause mortality in a high-burden malaria and HIV region of Kenya.Tropical medicine and health · 2022Article
- Genomic and Genetic Approaches to Deciphering Acute Respiratory Distress Syndrome Risk and Mortality.Antioxidants & redox signaling · 2019Review
- Relation between Red Cell Distribution Width and Mortality in Critically Ill Patients with Acute Respiratory Distress Syndrome.BioMed research international · 2019Article
- The Basic Science and Molecular Mechanisms of Lung Injury and Acute Respiratory Distress Syndrome.International anesthesiology clinics · 2018Review
- Fifty Years of Research in ARDS. Genomic Contributions and Opportunities.American journal of respiratory and critical care medicine · 2017Review
- Novel translational approaches to the search for precision therapies for acute respiratory distress syndrome.The Lancet. Respiratory medicine · 2017Review
- A targeted approach to genome-wide studies reveals new genetic associations with central corneal thickness.Molecular vision · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
PURPOSE/
aimAcute Respiratory Distress Syndrome (ARDS) is an important clinical and public health problem. Why some at-risk individuals develop ARDS and others do not is unclear but may be related to differences in inflammatory and cell signaling systems. The Receptor for Advanced Glycation Endproducts (RAGE) and Granulocyte-Monocyte Stimulating Factor (GM-CSF) pathways have recently been implicated in pulmonary pathophysiology; whether genetic variation within these pathways contributes to ARDS risk or outcome is unknown. MATERIALS AND
methodsWe studied 842 patients from three centers in Utah and 14 non-Utah ARDS Network centers. We studied patients at risk for ARDS and patients with ARDS to determine whether Single Nucleotide Polymorphisms (SNPs) in the RAGE and GM-CSF pathways were associated with development of ARDS. We studied 29 SNPs in 5 genes within the two pathways and controlled for age, sepsis as ARDS risk factor, and severity of illness, while targeting a false discovery rate of ≤ 5%. In a secondary analysis we evaluated associations with mortality.
resultsOf 842 patients, 690 had ARDS, and 152 were at-risk. Sepsis was the risk factor for ARDS in 250 (30%) patients. When controlling for age, APACHE III score, sepsis as risk factor, and multiple comparisons, no SNPs were significantly associated with ARDS. In a secondary analysis, only rs743564 in CSF2 approached significance with regard to mortality (OR 2.17, unadjusted p = 0.005, adjusted p = 0.15).
conclusionsCandidate SNPs within 5 genes in the RAGE and GM-CSF pathways were not significantly associated with development of ARDS in this multi-centric cohort.
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