ArticleThe World Allergy Organization journal2024
A multi-omics Mendelian randomization identifies putatively causal genes and DNA methylation sites for asthma.
Article in The World Allergy Organization journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Causal relationships between hundreds of plasma metabolites and PTSD: a bidirectional mendelian randomization study.BMC psychiatry · 2025Pooled it
- Mitochondria-Related Pathogenic Genes in Paediatric Asthma: A Multi-Omics Mendelian Randomization Study.Journal of cellular and molecular medicine · 2026Article
- Nephroprotective Effects of Quercetin-Selenium Nanoparticles Against Glycerol-Induced AKI.International journal of molecular sciences · 2025Article
- Identifying therapeutic targets for allergic asthma through atopic dermatitis-associated genetic mechanisms.The journal of allergy and clinical immunology. Global · 2025Article
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5 authors.
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Abstract
Background: Asthma is a global chronic respiratory disease with complex pathogenesis. While current therapies offer some relief, they often fall short in effectively managing symptoms and preventing exacerbations for numerous patients. Thus, understanding its mechanisms and discovering new drug targets remains a pressing need for better treatment. Methods: Using the GEO dataset, we screened differentially expressed genes (DEGs) in asthma patients' blood. Employing Summary Data-based Mendelian Randomization (SMR) and Two-Sample Mendelian Randomization (TSMR), we pinpointed asthma causal genes, causal DNA methylation sites, and methylation sites affecting gene expression, cross validated with at least 2 large-scale GWAS from each source. We utilized colocalization for genetic associations, meta-analysis for data integration, two-step MR for methylation-gene-asthma mediation mechanism. Druggability was evaluated using Open Target, virtual screening, and docking. Results: Among the 954 DEGs found in asthma patients' blood, increased expression of CEP95 (discovery, OR_SMR = 0.94, 95% CI: 0.91-0.97), RBM6 (discovery, OR_SMR = 0.97, 95% CI: 0.95-0.99), and ITPKB (discovery, OR_SMR = 0.82, 95% CI: 0.74-0.92) in the blood decreased the risk of asthma, higher levels of HOXB-AS1 (discovery, OR_SMR = 1.05, 95% CI: 1.03-1.07), ETS1 (discovery, OR_SMR = 1.62, 95% CI: 1.29-2.04), and JAK2 (discovery, OR_SMR = 1.13, 95% CI: 1.06-1.21) in the blood increased the risk of asthma. Additionally, a total of 8 methylation sites on ITPKB, ETS1, and JAK2 were identified to influence asthma. An increase in methylation at site cg16265553 raised the risk of asthma partially by suppressing ITPKB expression. Similarly, increased methylation at cg13661497 reduced the asthma risk totally by suppressing JAK2 expression. The impact of CEP95, HOXB-AS1, and RBM6 expressions on asthma was further confirmed in lung tissues. Except for HOXB-AS1, all the other genes were potential druggable targets. Conclusion: Our study highlighted that specific gene expressions and methylation sites significantly influence asthma risk and revealed a potential methylation-to-gene-to-asthma mechanism. This provided pivotal evidence for future targeted functional studies and the development of preventive and treatment strategies.
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