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Association of the ATG9B gene polymorphisms with coronary artery disease susceptibility: A case-control study

Introduction: Endothelial nitric oxide synthase (eNOS), the main regulator of cardiac cell functioning, is regulated post-transcriptionally by autophagy-related 9B (ATG9B) gene. The proper function of the heart is partly determined by the intact interaction of these molecules. The present study aime...

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Detalles Bibliográficos
Autores principales: Mehrabi Pour, Mahsa, Nasiri, Mahboobeh, Kamfiroozie, Hajar, Zibaeenezhad, Mohammad Javad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Tabriz University of Medical Sciences 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6669433/
https://www.ncbi.nlm.nih.gov/pubmed/31384404
http://dx.doi.org/10.15171/jcvtr.2019.19
Descripción
Sumario:Introduction: Endothelial nitric oxide synthase (eNOS), the main regulator of cardiac cell functioning, is regulated post-transcriptionally by autophagy-related 9B (ATG9B) gene. The proper function of the heart is partly determined by the intact interaction of these molecules. The present study aimed to investigate the effects of ATG9B rs2373929 and rs7830 gene polymorphisms on the predisposition to coronary artery disease (CAD). Methods: In this hospital-based case-control study, 150 patients with CAD compared with 150 healthy subjects for the genotype distributions of rs2373929 and rs7830 polymorphisms using T-ARMS PCR and ARMS PCR, respectively. Results: Considering rs2373929 polymorphism, increased risk of CAD observed in the presence of TT genotype (OR: 3.65; 95% CI: 1.77-7.53; P < 0.001) and also in the recessive model for T allele (OR: 3.41; 95% CI: 1.76- 6.60; P < 0.001). The frequency of the T allele was higher in cases compared to controls (OR: 1.71; 95% CI: 1.24-2.28; P = 0.001). The genotype and allele frequencies of the rs7830 polymorphism did not differ between the two study groups. Conclusion: The ATG9B gene rs2373929 polymorphism might involve in the pathogenesis of the CAD and can be considered as a screening molecular marker in the subjects prone to CAD.