ArticleHuman genomics2013
A study of the role of GATA4 polymorphism in cardiovascular metabolic disorders.
Article in Human genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prevalence, risk factors, and interventions for obesity in Saudi Arabia: A systematic review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2022Pooled it
- The intersection of disorders of sex development and cardiovascular diseases.Biology of sex differences · 2026Review
- Targeting senescence and GATA4 in age-related cardiovascular disease: a comprehensive approach.Biogerontology · 2025Review
- Characterization of genomic variants associated with congenital heart disease in patients from southwestern Colombian.Heliyon · 2024Article
- Loss of GATA4 C-Terminus by p.S335X Mutation Modulates Coronary Artery Vascular Smooth Muscle Cell Phenotype.Mediators of inflammation · 2021Article
- GATA4 protects against hyperglycemia‑induced endothelial dysfunction by regulating NOX4 transcription.Molecular medicine reports · 2018Article
- The effects of transfection reagent polyethyleneimine (PEI) and non-targeting control siRNAs on global gene expression in human aortic smooth muscle cells.BMC genomics · 2016Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe study was designed to evaluate the association of GATA4 gene polymorphism with coronary artery disease (CAD) and its metabolic risk factors, including dyslipidaemic disorders, obesity, type 2 diabetes and hypertension, following a preliminary study linking early onset of CAD in heterozygous familial hypercholesterolaemia to chromosome 8, which harbours the GATA4 gene.
resultsWe first sequenced the whole GATA4 gene in 250 individuals to identify variants of interest and then investigated the association of 12 single-nucleotide polymorphisms (SNPs) with the disease traits using Taqman chemistry in 4,278 angiographed Saudi individuals. Of the studied SNPs, rs804280 (1.14 (1.03 to 1.27); p = 0.009) was associated with CAD (2,274 cases vs 2,004 controls), hypercholesterolaemia (1,590 vs 2,487) (1.61 (1.03-2.52); p = 0.037) and elevated low-density lipoprotein-cholesterol (hLDLC) (575 vs 3,404) (1.87 (1.10-3.15); p = 0.020). Additionally, rs3729855_T (1.52 (1.09-2.11; p = 0.013)) and rs17153743 (AG + GG) (2.30 (1.30-4.26); p = 0.005) were implicated in hypertension (3,312 vs 966), following adjustments for confounders. Furthermore, haplotypes CCCGTGCC (χ2 = 4.71; p = 0.041) and GACCCGTG (χ2 = 3.84; p = 0.050) constructed from the SNPs were associated with CAD and ACCCACGC (χ2 = 6.58; p = 0.010) with myocardial infarction, while hypercholesterolaemia (χ2 = 3.86; p = 0.050) and hLDLC (χ2 = 4.94; p = 0.026) shared the AACCCATGT, and AACCCATGTC was associated with hLDLC (χ2 = 4.83; p = 0.028). A 10-mer GACCCGCGCC (χ2 = 7.59; p = 0.006) was associated with obesity (1,631 vs 2,362), and the GACACACCC (χ2 = 4.05; p = 0.044) was implicated in type 2 diabetes mellitus 2,378 vs 1,900).
conclusionOur study implicates GATA4 in CAD and its metabolic risk traits. The finding also points to the possible involvement of yet undefined entities related to GATA4 transcription activity or gene regulatory pathways in events leading to these cardiovascular disorders.
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