Trial reportPloS one2021
Molecular genetic study on GATA5 gene promoter in acute myocardial infarction.
Trial report in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 17 citations in OpenAlex.
- Uncovering potential diagnostic biomarkers of acute myocardial infarction based on machine learning and analyzing its relationship with immune cells.BMC cardiovascular disorders · 2023Article
- Overexpression of GATA5 Inhibits Prostate Cancer Progression by Regulating PLAGL2 via the FAK/PI3K/AKT Pathway.Cancers · 2022Article
- Article
- NONMMUT140591.1 may serve as a ceRNA to regulate Gata5 in UT-B knockout-induced cardiac conduction block.Open life sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myocardial infarction (AMI) is a severe type of coronary artery disease, caused by coronary occlusion and followed by cardiac ischaemia. GATA binding protein 5 (GATA5) is an important member of GATA family and plays an important role in vascular inflammation, endothelial function, oxidative stress and cell metabolism. Previous studies have shown that the DNA sequence variants (DSVs) in GATA4 and GATA6 promoter can increase susceptibility to AMI. In this study, we explored the relationship between GATA5 promoter and AMI for the first time, hoping to provide a new genetic basis for understanding the pathogenesis of AMI.
methodsGATA5 promoter was sequenced in 683 individuals (332 AMI patients and 351 controls). The transcriptional activity of the GATA5 promoter with or without DSVs in HEK-293 cells, H9c2 cells and primary neonatal rat cardiomyocytes were examined by Promega Dual-Luciferase® Reporter Assay system. Electrophoretic mobility shift assay (EMSA) was performed to explore whether the DSVs interfered with the binding of transcription factors (TFs).
resultsNine mutations have been found in GATA5 promoter, eight of them evidently altered the transcriptional activity of the GATA5 promoter, five of them disrupted the binding of TFs (such as farnesoid X receptor). Furthermore, haplotype AT (across rs80197101 and rs77067995) is a dangerous haplotype of AMI. Genotype GA and allele A of rs80197101 and genotype CT and allele T of rs77067995 are the risk factors of AMI.
conclusionsDSVs in GATA5 promoter can increase susceptibility to AMI. But the mechanism remains to be verified in vivo.
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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.