Cargando…

A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Merzah, Mohammed, Póliska, Szilárd, Balogh, László, Sándor, János, Szász, István, Natae, Shewaye, Fiatal, Szilvia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10530857/
https://www.ncbi.nlm.nih.gov/pubmed/37762221
http://dx.doi.org/10.3390/ijms241813920
_version_ 1785111583956926464
author Merzah, Mohammed
Póliska, Szilárd
Balogh, László
Sándor, János
Szász, István
Natae, Shewaye
Fiatal, Szilvia
author_facet Merzah, Mohammed
Póliska, Szilárd
Balogh, László
Sándor, János
Szász, István
Natae, Shewaye
Fiatal, Szilvia
author_sort Merzah, Mohammed
collection PubMed
description 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.
format Online
Article
Text
id pubmed-10530857
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-105308572023-09-28 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 Int J Mol Sci Article 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. MDPI 2023-09-10 /pmc/articles/PMC10530857/ /pubmed/37762221 http://dx.doi.org/10.3390/ijms241813920 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Merzah, Mohammed
Póliska, Szilárd
Balogh, László
Sándor, János
Szász, István
Natae, Shewaye
Fiatal, Szilvia
A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients
title A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients
title_full A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients
title_fullStr A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients
title_full_unstemmed A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients
title_short A Transcriptomic Analysis of Smoking-Induced Gene Expression Alterations in Coronary Artery Disease Patients
title_sort transcriptomic analysis of smoking-induced gene expression alterations in coronary artery disease patients
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10530857/
https://www.ncbi.nlm.nih.gov/pubmed/37762221
http://dx.doi.org/10.3390/ijms241813920
work_keys_str_mv AT merzahmohammed atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT poliskaszilard atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT baloghlaszlo atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT sandorjanos atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT szaszistvan atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT nataeshewaye atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT fiatalszilvia atranscriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT merzahmohammed transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT poliskaszilard transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT baloghlaszlo transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT sandorjanos transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT szaszistvan transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT nataeshewaye transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients
AT fiatalszilvia transcriptomicanalysisofsmokinginducedgeneexpressionalterationsincoronaryarterydiseasepatients