ArticleMedicine2025
Causal relationship between uterine fibroids and cardiovascular disease: A two-sample Mendelian randomization study.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The Relationship Between Immune Cells and Uterine Fibroids: A Bidirectional Mendelian Randomization Study.International journal of women's health · 2026Article
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
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have indicated that patients with uterine fibroids (UF) may have an elevated risk of cardiovascular disease (CVD), although the causal relationship between UF and CVD remains unclear. In this Mendelian randomization (MR) study, we aimed to investigate the causal association between genetic susceptibility to UF and the risk of developing CVD. We extracted summary statistics for single nucleotide polymorphisms associated with UF and 5 CVDs from multiple databases for further analysis. First, we used linkage disequilibrium score regression to assess the genetic correlation across the genome. Next, we performed univariate MR (UVMR), and to ensure the robustness of our results, we conducted sensitivity analyses using several methods. Additionally, we applied multivariable MR (MVMR) to adjust for potential confounders. The linkage disequilibrium score regression results showed that there was no genetic correlation between UF and coronary heart disease, myocardial infarction (MI), atrial fibrillation, heart failure, cardioembolic stroke (CES). The UVMR revealed a significant association between UF and CES (OR = 1.113, 95% confidence interval [CI]: 1.018-1.218, P = .019, PFDR = .047) and a suggestive causal relationship between UF and MI (OR = 0.943, 95% CI: 0.899-0.989, P = .015, PFDR = .075). In the MVMR analysis, after adjusting for a range of potential confounders, the causal relationships between UF and both CES (OR = 1.104, 95% CI = 1.012-1.205, P = .027) and MI (OR = 0.935, 95% CI = 0.882-0.992, P = .025) remained significant. Our study found that UF increase the risk of CES but decrease the risk of MI, providing a theoretical basis for further research into the underlying mechanisms.
Indexed as
Identifiers
What 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.