SynthesisClinical cardiology2025
Mapping Gastroesophageal Reflux Disease and Coronary Artery Disease: A Comprehensive Analysis of Multivariable Mendelian Randomization and Shared Genetic Etiology.
Synthesis in Clinical cardiology, 2025. 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.
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
aimsWe employed a robust genetic approach to provide a better understanding of whether Gastroesophageal reflux disease (GERD) contributes to coronary artery disease (CAD) risk from a genetic perspective.
methodsMultivariable Mendelian Randomization (MVMR) was applied to explore causal links between GERD and CAD using genetic instruments derived from genome-wide association studies (GWAS). The MVMR models were adjusted for key metabolic confounders, including low-density lipoprotein cholesterol (LDL-C), body mass index (BMI), systolic blood pressure (SBP), and glycated hemoglobin (HbA1c). Genetic correlations were estimated using linkage disequilibrium score regression. Cross-trait meta-analyses, Heritability Estimation from Summary Statistics (ρ-HESS) and colocalization analyses were performed to identify pleiotropic genes and shared genetic loci, elucidating the genetic relationship between GERD and CAD.
resultsGenetically predicted GERD was found to be causally linked with CAD (rg = 0.38, P = 2.37E-52), independent of metabolic risk factors, including LDL-C, BMI, SBP, and HbA1c (odds ratio: 1.24, 95% CI: 1.02-1.52, p < 0.05). Cross-trait meta-analyses identified eight novel pleiotropic single nucleotide polymorphisms, four of which were independent of metabolic confounders, including rs11764337 in MAD1L1, rs2240326 in RBM5, rs9615905 in FAM19A5, and rs9837341 in BSN. ρ-HESS and colocalization analysis further revealed shared genetic loci for GERD and CAD, specifically rs4643373 in IGF2BP1 (located in chr17: 45876022-47517400 and posterior probability for H4 > 0.75).
conclusionsGERD is identified as an independent risk factor for CAD. The discovery of shared genetic loci provides novel insights into the genetic mechanisms underlying GERD and CAD, with IGF2BP1 emerging as a potential therapeutic target for intervention.
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