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
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

835-843

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2023 Sociedade Portuguesa de Cardiologia. Publicado por Elsevier España, S.L.U. All rights reserved.

Auteurs

Vahid Akbari Kordkheyli (V)

Clinical Biochemistry, Human Genetic Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.

Arash Poursheikhani (A)

Legal Medicine Research Center, Legal Medicine Organization, Tehran, Iran.

Seyed Hasan Sharobandi (SH)

Atherosclerosis Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.

Sayed Mostafa Hosseini (SM)

Molecular Genetics, Human Genetic Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran. Electronic address: smhosseini@bmsu.ac.ir.

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Classifications MeSH