ArticlePrenatal diagnosis2025
mRNA Expression to Assess Hypoxia and Angiogenesis in Decidual Tissue of Term Fetuses With a Congenital Heart Disease.
Article in Prenatal diagnosis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- mRNA Expression to Assess Hypoxia and Angiogenesis in Decidual Tissue of Term Fetuses With a Congenital Heart Disease.Prenatal diagnosis · 2025Article
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8 authors.
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Abstract
objectiveDelayed fetal neurodevelopment, lower birth weight, and placental abnormalities are related to congenital heart defects (CHD). We explored mRNA expression assessment of candidate genes related to fetal hypoxia and angiogenesis in decidual tissues of pregnancies with different types of fetal CHD, classified based on aortic flow and oxygenation.
methodIn this prospective case-control study, mRNA expression was assessed for 18 candidate genes related to fetal hypoxia and angiogenesis in decidual (maternal) tissues of fetal simple transposition of the great arteries (TGA) (n = 14) and left sided CHD (n = 13) and in healthy controls (n = 31). Cases with a fetal syndrome/genetic abnormality, termination of pregnancy, intra-uterine fetal demise, or multiple pregnancies were excluded.
resultsThere were no significant differences in gene expression of the candidate genes between CHD cases and controls and between cases with fetal simple TGA and cases with fetal left sided CHD. Clustering analysis did not differentiate subgroups within the study population.
conclusionsFetal hypoxia and altered angiogenesis on the level of mRNA expression in decidual tissue were not significantly different between CHD cases and controls and between cases with fetal simple TGA and cases with fetal left sided CHD. We hypothesize that other (angio) genetic and molecular pathways lead to morphological placental alterations in pregnancies with fetal CHD.
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