ArticleThe Journal of allergy and clinical immunology2022
A genomic approach identifies sRAGE as a putatively causal protein for asthma.
Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Hyperglycemia, receptor for advanced glycation end products, and small airways dysfunction in asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2026Article
- Low sRAGE Level is Associated with Increased Future Exacerbation Risk in Mild-to-Moderate COPD and Patients with Chronic Bronchitis Symptoms.International journal of chronic obstructive pulmonary disease · 2026Observational
- Integrative Mendelian randomization reveals the soluble receptor for advanced glycation end products as protective in relation to rheumatoid arthritis.Scientific reports · 2023Article
- RAGE contributes to allergen driven severe neutrophilic airway inflammationFrontiers in immunology · 2023Article
- Assessment of Fraction of Exhaled Nitric Oxide and Soluble Receptor for Advanced Glycation End Products Biomarkers for Jordanian Asthmatic Children.Journal of asthma and allergy · 2023Article
- Association of 71 cardiovascular disease-related plasma proteins with pulmonary function in the community.PloS one · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAsthma is a complex respiratory condition caused by environmental and genetic factors. Although lower concentrations of the anti-inflammatory protein soluble receptor for advanced glycation end products (sRAGE) have been associated with asthma in humans and mouse models, it is uncertain whether sRAGE plays a causal role in asthma.
objectiveWe designed a 2-stage study of sRAGE in relation to asthma with association analysis in FHS participants as well as causal inference testing using Mendelian randomization (MR).
methodsWe measured plasma levels of sRAGE and performed cross-sectional analysis to examine the association between plasma sRAGE concentration and asthma status in 6546 FHS participants. We then used sRAGE protein advanced glycation end products (pQTLs) derived from a genome-wide association study of plasma sRAGE levels in ∼7000 FHS participants with UK Biobank asthma genome-wide association study in MR to consider sRAGE as a putatively causal protein for asthma. We also performed replication MR using an externally derived sRAGE pQTL from the INTERVAL study. Last, we conducted colocalization using cis-pQTL variants at the advanced glycosylation end-product specific receptor (AGER) locus with variants from the UK Biobank asthma genome-wide association study.
resultsAssociation analysis revealed that each 1 SD increment in sRAGE concentration was associated with a 14% lower odds of asthma in FHS participants (95% CI 0.76-0.96). MR identified sRAGE as putatively causal for and protective against asthma on the basis of self-reported (odds ratio [per 1 SE increment in inverse-rank-normalized sRAGE] = 0.97, 95% CI 0.95-0.99; P = .005) and doctor-diagnosed asthma (odds ratio = 0.97, 95% CI 0.95-0.99; P = .011).
conclusionThrough this genomic approach, we identified sRAGE as a putatively causal, biologically important, and protective protein in relation to asthma. Functional studies in cell/animal models are needed to confirm our findings.
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