ArticleInternational journal of clinical pharmacy2026
Genetic variation in anti-diabetic drug targets and risk of atrial fibrillation: a drug-target mendelian randomization study.
Article in International journal of clinical pharmacy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
introductionAtrial fibrillation (AF) is a common cardiac arrhythmia with limited options for upstream prevention. While several anti-diabetic drugs have shown cardiovascular benefits, their potential role in modifying AF risk remains unclear.
aimThis study aimed to evaluate the causal relationship between genetically proxied antidiabetic drug targets and the risk of AF using a drug-target Mendelian randomization (MR) approach.
methodA two-sample MR analysis was conducted to investigate the association between genetic variants related to antidiabetic drug targets and AF. Thirty-eight FDA-approved glucose-lowering agents were identified, and their targets were extracted from the ChEMBL (Chemical Biology Database and Information System) database. Protein quantitative trait loci (pQTL) data from a large plasma proteome GWAS (Genome-Wide Association Study) were used to construct instrumental variables. Positive control testing was conducted to confirm that the selected drug targets were significantly associated with diabetes, using summary statistics from the UK Biobank, FinnGen, and other GWAS datasets. Causal effects on AF were evaluated using multiple independent GWAS cohorts for replication. MR methods included inverse-variance weighted (IVW), MR-Egger, and weighted median approaches with sensitivity analyses for pleiotropy and heterogeneity.
resultsThe alpha-glucosidase inhibitor miglitol was causally associated with a reduced risk of AF. Specifically, miglitol was shown to inhibit lactase (LCT), a protein whose elevated levels were associated with increased AF risk (IVW, OR = 1.013; 95%CI, 1.007-1.018; P = 2.37 × 10⁻
conclusionThis study provides novel genetic evidence suggesting that miglitol may reduce AF risk through lactase inhibition. These findings highlight a potential opportunity for drug repurposing for cardiovascular prevention, particularly for clinical pharmacists managing patients with higher risks in cardiovascular outcomes meanwhile with type 2 diabetes. Further mechanistic and clinical studies are warranted to confirm these observations and explore their translational value in practice.
Indexed as
Identifiers
41264079What Socratic holds
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 Socratic graph.