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A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients.
Merzah, Mohammed; Póliska, Szilárd; Balogh, László; Sándor, János; Szász, István; Natae, Shewaye; Fiatal, Szilvia.
Afiliación
  • Merzah M; Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
  • Póliska S; Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
  • Balogh L; Cardiology and Cardiac Surgery Clinic, University of Debrecen, H-4032 Debrecen, Hungary.
  • Sándor J; Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
  • Szász I; ELKH-DE Public Health Research Group, Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
  • Natae S; Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
  • Fiatal S; ELKH-DE Public Health Research Group, Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
Int J Mol Sci ; 24(18)2023 Sep 10.
Article en En | MEDLINE | ID: mdl-37762221
Smoking is a well established risk factor for coronary artery disease (CAD). Despite this, there have been no previous studies investigating the effects of smoking on blood gene expression in CAD patients. This single-centre cross-sectional study was designed with clearly defined inclusion criteria to address this gap. We conducted a high-throughput approach using next generation sequencing analysis with a single-end sequencing protocol and a read length of 75-cycles. Sixty-one patients with a median age of 67 years (range: 28-88 years) were recruited, and only 44 subjects were included for further analyses. Our investigation revealed 120 differentially expressed genes (DEGs) between smokers and nonsmokers, with a fold change (FC) of ≥1.5 and a p-value < 0.05. Among these DEGs, 15 were upregulated and 105 were downregulated. Notably, when applying a more stringent adjusted FC ≥ 2.0, 31 DEGs (5 upregulated, annotated to immune response pathways, and 26 downregulated, involving oxygen and haem binding or activity, with FDR ≤ 0.03) remained statistically significant at an alpha level of <0.05. Our results illuminate the molecular mechanisms underlying CAD, fortifying existing epidemiological evidence. Of particular interest is the unexplored overexpression of RCAN3, TRAV4, and JCHAIN genes, which may hold promising implications for the involvement of these genes in CAD among smokers.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Enfermedad de la Arteria Coronaria / Fumar Tipo de estudio: Observational_studies / Prevalence_studies / Risk_factors_studies Límite: Adult / Aged / Aged80 / Humans / Middle aged Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article País de afiliación: Hungria

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Enfermedad de la Arteria Coronaria / Fumar Tipo de estudio: Observational_studies / Prevalence_studies / Risk_factors_studies Límite: Adult / Aged / Aged80 / Humans / Middle aged Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article País de afiliación: Hungria