ArticleJournal of pharmacy & bioallied sciences2024
Vascular Inflammatory Genes as Predictors of Preeclampsia: A Systematic Review.
Article in Journal of pharmacy & bioallied sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Trophoblast Function in Preeclampsia: Decoding the Mechanistic Roles of Coding and Non-Coding Genes.International journal of molecular sciences · 2025Review
- The gut-placenta axis in preeclampsia: unraveling the regulatory network and clinical prospects in pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Preeclampsia, a condition causing new-onset hypertension and proteinuria after 20 weeks of gestation, is a significant cause of maternal and fetal morbidity and mortality. The pathogenesis of preeclampsia is complex, involving an interplay of vascular inflammation and angiogenic imbalance. This systematic review and meta-analysis aims to elucidate the role of key vascular inflammatory candidate genes-VEGF, TNF-α, IL-10, and LPL-in the onset of preeclampsia. Methodology: We conducted a comprehensive literature search across PubMed, Embase, and Cochrane databases, identifying case-control and cohort studies that examined the association between these genetic variants and preeclampsia. Results: Our meta-analysis reveals significant associations between preeclampsia and polymorphisms in the VEGF, TNF-α, IL-10, and LPL genes, with pooled odds ratios indicating increased risk for the VEGF -2578C>A, VEGF -1154G>A, TNF-α -308G>A, IL-10 -819C>T, and LPL Ser447Ter variants. Conclusion: These findings suggest that genetic predispositions in vascular inflammatory pathways may contribute to the development of preeclampsia, offering potential targets for early detection and therapeutic intervention. Further research is warranted to explore the molecular mechanisms by which these genetic variants influence the pathogenesis of preeclampsia and to develop targeted prevention strategies.
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Registered trials
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