Observational studyJournal of human hypertension2025
Exploration of potential therapeutic target genes for preeclampsia through genetic analysis.
Observational study in Journal of human hypertension, 2025. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a prevalent and severe pregnancy-related complication, for which effective intervention targets remain limited, posing significant risks to maternal and fetal health. This study aimed to identify potential therapeutic target genes through genetic analyses. Specifically, we utilized cis-expression quantitative trait loci (cis-eQTL) of druggable genes derived from blood samples obtained from the eQTLGen consortium as exposure data. Subsequently, Mendelian randomization (MR) analysis was conducted to explore causal associations between these druggable genes and PE. Functional enrichment analysis, Summary-data-based MR (SMR), and colocalization analysis were employed to validate the identified genes. MR results revealed 17 druggable genes significantly associated with PE after multiple testing correction (FDR < 0.05). Functional enrichment analysis indicated that these genes are involved in key biological processes such as leukocyte proliferation and activation, immune response regulation, and the metabolism of water-soluble vitamins. Additionally, they were found to participate in several critical signaling pathways, including the complement and coagulation cascades, the renin-angiotensin system, and folate biosynthesis. SMR and colocalization analyses further confirmed the causal relationships between PE and five genes-TESK2, LNPEP, CD320, NELL2, and SF3B3. Moreover, single-cell RNA sequencing data supported the association between the expression levels of TESK2, CD320, and SF3B3 and the development of PE. This study provides preliminary evidence identifying several potential genetic targets that may help reduce the risk of PE from a genomic perspective. These findings offer novel scientific insights and research directions for future drug development and the optimization of therapeutic strategies aimed at managing and preventing PE.
Indexed as
Identifiers
40715499What 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.