ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Genetic Correlation and Causal Inference Between Female Fat Distribution and Preeclampsia: An Integrative Genomic Study.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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
6 authors.
Funding
Abstract
Preeclampsia (PE) is a major cause of maternal and perinatal morbidity. Because abnormal fat distribution is closely related to metabolic dysfunction, vascular injury, and hypertensive disorders during pregnancy, clarifying its genetic relationship with PE may improve our understanding of adverse pregnancy outcomes. Here, we investigated the shared genetic architecture between PE and waist-hip ratio adjusted for body mass index (WHRadjBMI) by integrating large-scale genome-wide association study (GWAS) summary statistics for female WHRadjBMI from the GIANT consortium (n ≈ 700 000) and PE from FinnGen R11 (7955 cases and 124 764 controls). Analyses included genome-wide genetic correlation, polygenic overlap, local genetic correlation, cross-trait GWAS meta-analysis, tissue/cell type enrichment, functional annotation, and Mendelian randomization, using tools including linkage disequilibrium score regression (LDSC), MiXeR, LAVA, ρ-HESS, MTAG, CPASSOC, and conjunctional false discovery rate (conjFDR). We identified approximately 0.5 k shared causal variants; MiXeR detected a modest but significant polygenic overlap (rg = 0.08, p = 0.006), whereas LDSC showed no significant genome-wide correlation. A shared genetic locus near MTHFR-CLCN6 (rs17367504) was detected, consistent with known PE biology. Enrichment analyses implicated VEGFA-driven vascular and immune processes, with uterine pericytes displaying the strongest shared cell-type enrichment. Mendelian randomization supported a causal effect of WHRadjBMI on PE (IVW: p = 2.7 × 10
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.