SynthesisCardiovascular therapeutics2026
Oxidative Stress-Related Genome-Wide Mendelian Randomization Identifies Causal Genes for Coronary Artery Disease.
Synthesis in Cardiovascular therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Oxidative Stress-Related Genome-Wide Mendelian Randomization Identifies Causal Genes for Coronary Artery Disease.Cardiovascular therapeutics · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Although oxidative stress (OS) links to the pathogenesis of coronary artery disease (CAD), its underlying genetic mechanisms remain unclear. Through summary data-based Mendelian randomization (SMR) and colocalization, this research seeks to assess the potential causal links between OS-related genes and CAD. Summary-level data on the methylation, expression, and protein abundance levels of OS-related genes were obtained from the corresponding quantitative trait loci (QTL) studies. We obtained genome-wide association study summary statistics for CAD from a previous study (discovery), the FinnGen and UK Biobank (replication). Two-sample MR analysis was conducted to verify the associations between key genes expressions and meta-analysis cohort of CAD risk. Mediation analysis was conducted to evaluate the mediating role of gene expression variation in the causal pathway linking methylation levels of key loci to the risk or progression of the disease. We identified 35 methylation loci, 7 genes, and 12 proteins in the discovery cohort. By integrating multiomic data, we identified SMARCA4, NAGLU, SREBF1, RPTOR, and HLA-B as potential causal targets associated with CAD. The two-sample MR analysis once again confirmed that the expressions of the SMARCA4, SREBF1, and HLA-B genes in the meta-analysis cohort showed a significant association with the risk of CAD, and this association was consistent with the direction of the SMR. Furthermore, both the expression and methylation of SMARCA4 were positively associated with CAD, and the direct and indirect effects of SMARCA4 methylation were confirmed. In summary, our results identified potential causal associations between SMARCA4, NAGLU, SREBF1, RPTOR, HLA-B, and CAD. The findings highlight the necessity for further exploration into the underlying etiology of CAD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.