ArticlePediatric cardiology2017
A Genetic Variant in FIGN Gene Reduces the Risk of Congenital Heart Disease in Han Chinese Populations.
Article in Pediatric cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Downregulation of miR-194-5p impairs cardiomyocyte proliferation and differentiation through targeting Fign in congenital heart disease.Molecular and cellular biochemistry · 2026Article
- Decoding Epilepsy: Prickle2 and Multifaceted Molecular Pathway Connections.Current pharmaceutical design · 2025Review
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Genomic frontiers in congenital heart disease.Nature reviews. Cardiology · 2022Review
- FIGNL1 promotes non‑small cell lung cancer cell proliferation.International journal of oncology · 2021Observational
- Associations between IL-6 Variations and Congenital Heart Disease Incidence among Chinese Han People.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Distinct subtypes of polycystic ovary syndrome with novel genetic associations: An unsupervised, phenotypic clustering analysis.PLoS medicine · 2020Article
- Race-specific alterations in DNA methylation among middle-aged African Americans and Whites with metabolic syndrome.Epigenetics · 2020Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital heart disease (CHD) is one of the most common birth anomalies worldwide. Folate deficiency is an independent risk factor for CHD. Genome-wide association studies (GWAS) revealed that human folate level could be significantly influenced by fidgetin (FIGN), methylenetetrahydrofolate reductase (MTHFR), prickle homolog 2 (PRICKLE2), synaptotagmin 9 (SYT9), gamma-aminobutyric acid B receptor 2 (GABBR2), and alkaline phosphatase (ALPL) genes. The association between the above-mentioned six variants and CHD was examined in the two independent case-control studies in a total of 868 CHD patients and 931 healthy controls. Our results showed that the G > C (rs2119289) variant in intron 4 of FIGN led to a significant reduction of CHD susceptibility in both the separate and combined case-control studies (allele distribution P < 0.001, genotype distribution P < 0.001). Specifically, by analyzing the combined samples, we observed that the risks of CHD in individuals carrying the heterozygous G/C and homozygous C/C genotypes were reduced by 45% (adjusted OR 0.55, 95% CI 0.47-0.67) and 66% (adjusted OR 0.34, 95% CI 0.23-0.50), respectively, in comparison with individuals carrying the wild-type G/G genotype. Our findings have demonstrated that the C allele of variant rs2119289 of FIGN gene is an important genetic marker for decreased CHD risk. Considering that the rs2119289 of FIGN gene is related to the appropriate folate level, FIGN might play an important role in CHD by upregulating plasma folate concentration during embryo heart development. This work provides a new insight for risk assessment of CHD.
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