ArticleJournal of human hypertension2016
The relationship between circulating tissue transglutaminase, soluble fms-like tyrosine kinase-1, soluble endoglin and vascular endothelial growth factor in pre-eclampsia.
Article in Journal of human hypertension, 2016. 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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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
3 citing papers in PubMed, 12 citations in OpenAlex.
- IL-6 Polymorphism as a Predisposing Genetic Factor for Gestational Diabetes or Preeclampsia Development in Pregnancy with Obesity in Relation to VEGF and VEGFF Receptor Gene Expression Modalities.Diagnostics (Basel, Switzerland) · 2024Article
- Soyghurt Potentially Controls the Level of sFlt1 and PLGF in Preeclampsia Maternal Serum-Induced Placental Trophoblast Cell in vitro.Journal of experimental pharmacology · 2024Article
- A risk factor-based predictive model for new-onset hypertension during pregnancy in Chinese Han women.BMC cardiovascular disorders · 2020Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a pregnancy-specific syndrome that causes substantial maternal and fetal morbidity and mortality. Increased production of antiangiogenic factors, soluble fms-like tyrosine kinase receptor-1 (sFlt-1) and soluble endoglin (sEng), as well as decreased circulating levels of free vascular endothelial growth factor (VEGF), contribute to the pathophysiology of PE. Our objective was to evaluate a novel placenta-related factor, tissue transglutaminase (tTG), in PE and to investigate the correlation among tTG and sFlt-1, sEng and VEGF levels in both normotensive pregnant patients and PE patients. A total of 205 pregnant primigravid women were recruited and divided into a normotensive group (n=100), a mild PE group (n=45) and a severe PE group (n=60). Circulating serum tTG, sFlt-1, sEng and free VEGF levels were determined using an enzyme-linked immunosorbent assay. The severe PE group showed higher levels of tTG, sFlt-1 and sEng than the mild PE and normotensive groups. Free VEGF levels were lower in the severe PE group than in the mild PE and normotensive groups. tTG correlated significantly with sFlt-1, sEng and VEGF in the PE groups, whereas this correlation was not observed in the normotensive group. The tTG, sFlt-1, sEng and VEGF levels showed a significant correlation with mean arterial pressure in the PE groups but not in the normotensive group. The tTG, sFlt-1, sEng and VEGF levels correlated with the degree of proteinuria. Our results reveal that tTG is associated with sFlt-1, sEng and VEGF in the maternal circulation of PE patients, suggesting that tTG may have a role in the pathogenesis of PE.
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