SynthesisPediatric cardiology2014
Association between methionine synthase reductase A66G polymorphism and the risk of congenital heart defects: evidence from eight case-control studies.
Synthesis in Pediatric cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.
- Association between MTR A2756G polymorphism and susceptibility to congenital heart disease: A meta-analysis.PloS one · 2022Pooled it
- Environmental and Genetic Risk Factors of Congenital Anomalies: an Umbrella Review of Systematic Reviews and Meta-Analyses.Journal of Korean medical science · 2021Pooled it
- Parental Genetic Variants, MTHFR 677C>T and MTRR 66A>G, Associated Differently with Fetal Congenital Heart Defect.BioMed research international · 2017Trial
- Association of maternal folic acid supplementation and offspring MTRR gene polymorphism with congenital heart disease: a hospital-based case-control study in Han population.Journal of health, population, and nutrition · 2024Article
- Review
- A Common Polymorphism in theJournal of cardiovascular development and disease · 2022Article
- Association of Maternal Dietary Habits andFrontiers in pediatrics · 2021Article
- Are polymorphisms in MTRR A66G and MTHFR C677T genes associated with congenital heart diseases in Iranian population?Caspian journal of internal medicine · 2017Article
- Joint associations of folate, homocysteine and MTHFR, MTR and MTRR gene polymorphisms with dyslipidemia in a Chinese hypertensive population: a cross-sectional study.Lipids in health and disease · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methionine synthase reductase (MTRR) plays a major role in hyperhomocysteinemia, a risk factor related to the occurrence of congenital heart defects (CHDs). However, the associations between MTRR polymorphism and CHDs have been inconclusive. Thus, a metaanalysis of eight case-control studies was conducted to investigate 3,592 cases and 3,638 control subjects for MTRR A66G polymorphism to identify the association. Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were used to assess the strength of the association. The results showed that MTRR A66G polymorphism was associated with a higher CHD risk in the allele comparison (G vs A: OR 1.163; 95 % CI 1.016-1.330; P heterogeneity = 0.004), the homozygote comparison (GG vs AA: OR 1.332; 95 % CI 1.020-1.740; P heterogeneity = 0.035), and the dominant model (GG/AG vs AA: OR 1.218; 95 % CI 1.001-1.482; P heterogeneity = 0.001). In the subgroup analysis, this polymorphism was associated with CHDs in Asians in the homozygote comparison (GG vs AA: OR 1.427; 95 % CI 1.017-2.001; P heterogeneity = 0.019) and the allele comparison (G vs A: OR 1.203; 95 % CI 1.018-1.422; P heterogeneity = 0.002). In summary, the metaanalysis demonstrated that MTRR A66G polymorphism is a risk factor for CHDs. Further studies should be performed to investigate the association of plasma homocysteine levels, enzyme activity, parental genotypes, and vitamin complex intakes with the risk of CHDs.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.