ArticleFrontiers in endocrinology2023
Identification of key genes in the pathogenesis of preeclampsia via bioinformatic analysis and experimental verification.
Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Shared glycosylation-related molecular mechanism and immune infiltration patterns of fetal growth restriction and preeclampsia.Frontiers in immunology · 2026Article
- Placental transcriptome profiling in congenital Chagas disease: gene networks associated with transmission.Frontiers in cellular and infection microbiology · 2026Article
- AttBiomarker: unveiling preeclampsia biomarkers and molecular pathways through two-stage gene selection techniques and attention-based CNN with gene regulatory network analysis.Briefings in bioinformatics · 2025Article
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- The Deubiquitinating Enzyme USP4 Promotes Trophoblast Dysfunction by Stabilizing RYBP.Cell biochemistry and biophysics · 2025Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Preeclampsia (PE) is the primary cause of perinatal maternal-fetal mortality and morbidity. The exact molecular mechanisms of PE pathogenesis are largely unknown. This study aims to identify the hub genes in PE and explore their potential molecular regulatory network. Methods: We downloaded the GSE148241, GSE190971, GSE74341, and GSE114691 datasets for the placenta and performed a differential expression analysis to identify hub genes. We performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Disease Ontology (DO), Gene Set Enrichment Analysis (GSEA), and Protein-Protein Interaction (PPI) Analysis to determine functional roles and regulatory networks of differentially expressed genes (DEGs). We then verified the DEGs at transcriptional and translational levels by analyzing the GSE44711 and GSE177049 datasets and our clinical samples, respectively. Results: We identified 60 DEGs in the discovery phase, consisting of 7 downregulated genes and 53 upregulated genes. We then identified seven hub genes using Cytoscape software. In the verification phase, 4 and 3 of the seven genes exhibited the same variation patterns at the transcriptional level in the GSE44711 and GSE177049 datasets, respectively. Validation of our clinical samples showed that CADM3 has the best discriminative performance for predicting PE. Conclusion: These findings may enhance the understanding of PE and provide new insight into identifying potential therapeutic targets for PE.
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