SynthesisNaunyn-Schmiedeberg's archives of pharmacology2025
The relationship of NOS3 G894 T (rs1799983) gene polymorphism in the risk of congenital heart disease: a meta-analysis and bioinformatics study.
Synthesis in Naunyn-Schmiedeberg's archives of pharmacology, 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
10 authors.
Funding
Abstract
Nitric Oxide Synthase 3 (NOS3) G894 T (rs1799983) is an important regulator of cardiac development. Its role in congenital heart disease (CHD) has been extensively studied in recent years, but the results are contradictory. The aim of the present study was to better elucidate the relationship between the NOS3 G894 T gene polymorphism and susceptibility of CHD and its specific subtypes. A comprehensive literature search was conducted across several databases, including PubMed, Embase, Web of Science, Cochrane Library, CNKI, VIP, and Wan Fang. Meta-analysis was carried out using RevMan 5.4 software, and the odds ratio (OR) with 95% confidence intervals (CI) was used as the effect measure. Additionally, bioinformatics analysis was employed to explore the impact of NOS3 gene mutations on tetralogy of Fallot (TOF), using publicly available microarray datasets to assess NOS3 gene expression. Nine studies were included, comprising 1931 CHD cases and 1910 controls. Meta-analysis showed that the NOS3 G894 T polymorphism was associated with an increased risk of CHD in three genetic models: allele model (T vs G, OR = 1.31, 95% CI [1.02, 1.68], P = 0.04), homozygous model (TT vs GG, OR = 1.60, 95% CI [1.13, 2.26], P = 0.007), and dominant model (GT + TT vs GG, OR = 1.44, 95% CI [1.02, 2.05], P = 0.04). Subgroup analyses revealed a strong association with atrial septal defect (ASD), conotruncal defects (CTD), and septal defects, with the most significant correlation found for ASD. The NOS3 G894 T polymorphism was associated with the risk of CHD in ethnic subgroup, increasing the risk of CHD in white race. Bioinformatics analysis did not find significant differences in NOS3 gene expression between individuals with TOF. The NOS3 G894 T (rs1799983) gene polymorphism is significantly associated with the risk of CHD, with notable variations in this association across different regions and ethnic groups. The T allele increases the risk of CHD by 31% compared to the G allele. Additionally, this polymorphism is linked to specific CHD subtypes, especially ASD.
Indexed as
Identifiers
40571825What 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.