Analysis of KLF7 and KLF5 transcription factors gene variants in coronary artery disease.
Coronary artery disease
Doença arterial coronária
Fatores de transcrição
Genetic susceptibility
KLF
Polimorfismo
Polymorphism
Suscetibilidade genética
Transcriptional factors
Journal
Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology
ISSN: 2174-2030
Titre abrégé: Rev Port Cardiol
Pays: Portugal
ID NLM: 8710716
Informations de publication
Date de publication:
10 2023
10 2023
Historique:
received:
02
11
2022
revised:
03
03
2023
accepted:
08
03
2023
medline:
6
10
2023
pubmed:
3
6
2023
entrez:
2
6
2023
Statut:
ppublish
Résumé
Genetic susceptibility has a key role in the pathogenesis of coronary artery disease (CAD). KLF5 and KLF7 are transcriptional factors essential to cell development and differentiation. Their genetic variants have been associated with the risk of metabolic disorders. The present study aimed to evaluate the possible correlation of KLF5 (rs3812852) and KLF7 (rs2302870) single nucleotide polymorphisms (SNPs) with the risk of CAD for the first time in the world. The clinical trial study comprised 150 patients with CAD and 150 control subjects without CAD from the Iranian population. After blood sampling, deoxyribonucleic acid was extracted and genotyped using the Tetra Primer ARMS-PCR method and confirmed by Sanger sequencing. The KLF7 A/C genotypes and C allele frequency were meaningfully higher in the control group compared to the CAD+ group (p<0.05). No obvious association has been observed between KLF5 variants and CAD risk. However, the distribution of the AG genotype of KLF5 was statistically lower in CAD+ patients with diabetes than in CAD+ patients without diabetes (p<0.05). This study identified KLF7 SNP as a causative gene contributing to CAD, which presents novel insight into the molecular pathogenesis of the disease. It is, however, unlikely that KLF5 SNP has an essential role in the risk of CAD in the studied population.
Identifiants
pubmed: 37268267
pii: S0870-2551(23)00276-7
doi: 10.1016/j.repc.2023.03.017
pii:
doi:
Substances chimiques
Transcription Factors
0
KLF7 protein, human
0
Kruppel-Like Transcription Factors
0
KLF5 protein, human
0
Types de publication
Journal Article
Langues
eng
por
Sous-ensembles de citation
IM
Pagination
835-843Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2023 Sociedade Portuguesa de Cardiologia. Publicado por Elsevier España, S.L.U. All rights reserved.