ArticlePediatric cardiology2015
Association of TGFBR2 rs6785358 Polymorphism with Increased Risk of Congenital Ventricular Septal Defect in a Chinese Population.
Article in Pediatric cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Associations of TGFBR1 and TGFBR2 gene polymorphisms with the risk of hypospadias: a case-control study in a Chinese population.Bioscience reports · 2017Article
- Transforming growth factor-β signaling pathway-associated genes SMAD2 and TGFBR2 are implicated in metabolic syndrome in a Taiwanese population.Scientific reports · 2017Article
- The role of histone modification and a regulatory single-nucleotide polymorphism (rs2071166) in the Cx43 promoter in patients with TOF.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor beta receptor 2 (TGFBR2) plays a central role in normal heart development, and we investigated whether TGFBR2 polymorphism confers the risk of congenital ventricular septal defect (CVSD). The case-control study included 115 CVSD children and 188 healthy children in a Chinese population. TGFBR2 rs6785358 polymorphism was genotyped with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Enzyme-linked immunoassay (ELISA) was used to detect serum TGFBR2 levels. The genotype and allele frequency of TGFBR2 rs6785358 were significantly higher in the CVSD group than in the controls (all P < 0.05). The G allele carriers were associated with increased CVSD risk compared with the A allele carriers in CVSD group (OR 3.503, 95 % CI 2.670-4.596). Stratified analysis by gender revealed that the TGFBR2 rs6785358 genotype and allele frequency were significantly different between the CVSD case and controls, in both the male subgroup and the female subgroup (all P < 0.001). The G allele carriers were more susceptible to CVSD risk than the A allele carriers in both the male subgroup (OR 9.096, 95 % CI 5.398-15.33) and the female subgroup (OR 3.148, 95 % CI 1.764-5.618). Logistic regression analysis revealed that age, gender and genotype were associated with the risk of CVSD (all P < 0.05). The study findings revealed that TGFBR2 rs6785358 polymorphism contributes to CVSD susceptibility, and the G allele may increase the risk of CVSD.
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.