ArticlePacific Symposium on Biocomputing. Pacific Symposium on Biocomputing2025
Uterine fibroids show evidence of shared genetic architecture with blood pressure traits.
Article in Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Association between uterine fibroids and hypertension among women of reproductive age in Eastern Sudan: a matched case-control study.Scientific reports · 2026Article
- The Relationship Between Immune Cells and Uterine Fibroids: A Bidirectional Mendelian Randomization Study.International journal of women's health · 2026Article
- Renal dysfunction and metabolic alterations in patients with intracranial aneurysm rupture: an exploratory multivariable and principal component analysis.Frontiers in neurology · 2026Article
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7 authors.
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Abstract
Uterine leiomyomata (fibroids, UFs) are common, benign tumors in females, having an estimated prevalence of up to 80%. They are fibrous masses growing within the myometrium leading to chronic symptoms like dysmenorrhea, abnormal uterine bleeding, anemia, severe pelvic pain, and infertility. Hypertension (HTN) is a common risk factor for UFs, though less prevalent in premenopausal individuals. While observational studies have indicated strong associations between UFs and HTN, the biological mechanisms linking the two conditions remain unclear. Understanding the relationship between HTN and UFs is crucial because UFs and HTN lead to substantial comorbidities adversely impacting female health. Identifying the common underlying biological mechanisms can improve treatment strategies for both conditions. To clarify the genetic and causal relationships between UFs and BP, we conducted a bidirectional, two-sample Mendelian randomization (MR) analysis and evaluated the genetic correlations across BP traits and UFs. We used data from a multi-ancestry genome-wide association study (GWAS) meta-analysis of UFs (44,205 cases and 356,552 controls), and data from a cross-ancestry GWAS meta-analysis of BP phenotypes (diastolic BP [DBP], systolic BP [SBP], and pulse pressure [PP], N=447,758). We evaluated genetic correlation of BP phenotypes and UFs with linkage disequilibrium score regression (LDSC). LDSC results indicated a positive genetic correlation between DBP and UFs (Rg=0.132, p<5.0x10-5), and SBP and UFs (Rg=0.063, p<2.5x10-2). MR using UFs as the exposure and BP traits as outcomes indicated a relationship where UFs increases DBP (odds ratio [OR]=1.20, p<2.7x10-3). Having BP traits as exposures and UFs as the outcome showed that DBP and SBP increase risk for UFs (OR =1.04, p<2.2x10-3; OR=1.00, p<4.0x10-2; respectively). Our results provide evidence of shared genetic architecture and pleiotropy between HTN and UFs, suggesting common biological pathways driving their etiologies. Based on these findings, DBP appears to be a stronger risk factor for UFs compared to SBP and PP.
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