Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk
Background The role of inflammation in coronary artery disease (CAD) pathogenesis is well recognized. Moreover, smoking inhalation increases the activity of inflammatory mediators through an increase in leukotriene synthesis essential in atherosclerosis pathogenesis. Aim The aim of this study is to...
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| المؤلف الرئيسي: | |
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| مؤلفون آخرون: | , , , , , , , , , |
| التنسيق: | article |
| منشور في: |
2015
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| الوصول للمادة أونلاين: | http://hdl.handle.net/10725/3347 http://dx.doi.org/10.1007/s00011-015-0821-1 http://link.springer.com/article/10.1007/s00011-015-0821-1 |
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| _version_ | 1864513460988018688 |
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| author | Merhi, Mahmoud |
| author2 | Demirdjian, Sally Hariri, Essa Sabbah, Nada Youhanna, Sonia Ghassibe-Sabbagh, Michella Naoum, Joseph Haber, Marc Kanbar, Roy Zalloua, Pierre Khazen, Georges |
| author2_role | author author author author author author author author author author |
| author_facet | Merhi, Mahmoud Demirdjian, Sally Hariri, Essa Sabbah, Nada Youhanna, Sonia Ghassibe-Sabbagh, Michella Naoum, Joseph Haber, Marc Kanbar, Roy Zalloua, Pierre Khazen, Georges |
| author_role | author |
| dc.creator.none.fl_str_mv | Merhi, Mahmoud Demirdjian, Sally Hariri, Essa Sabbah, Nada Youhanna, Sonia Ghassibe-Sabbagh, Michella Naoum, Joseph Haber, Marc Kanbar, Roy Zalloua, Pierre Khazen, Georges |
| dc.date.none.fl_str_mv | 2015 2016-03-17T09:19:37Z 2016-03-17T09:19:37Z 2016-03-17 |
| dc.identifier.none.fl_str_mv | 1023-3830 http://hdl.handle.net/10725/3347 http://dx.doi.org/10.1007/s00011-015-0821-1 Merhi, M., Demirdjian, S., Hariri, E., Sabbah, N., Youhanna, S., Ghassibe-Sabbagh, M., ... & Chammas, E. (2015). Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk. Inflammation Research, 64(6), 415-422. http://link.springer.com/article/10.1007/s00011-015-0821-1 |
| dc.language.none.fl_str_mv | en |
| dc.relation.none.fl_str_mv | Inflammation Research |
| dc.rights.*.fl_str_mv | info:eu-repo/semantics/openAccess |
| dc.title.none.fl_str_mv | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| dc.type.none.fl_str_mv | Article info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/article |
| description | Background The role of inflammation in coronary artery disease (CAD) pathogenesis is well recognized. Moreover, smoking inhalation increases the activity of inflammatory mediators through an increase in leukotriene synthesis essential in atherosclerosis pathogenesis. Aim The aim of this study is to investigate the effect of “selected” genetic variants within the leukotriene (LT) pathway and other variants on the development of CAD. Methods CAD was detected by cardiac catheterization. Logistic regression was performed to investigate the association of smoking and selected susceptibility variants in the LT pathway including ALOX5AP, LTA4H, LTC4S, PON1, and LTA as well as CYP1A1 on CAD risk while controlling for age, gender, BMI, family history, diabetes, hyperlipidemia, and hypertension. Results rs4769874 (ALOX5AP), rs854560 (PON1), and rs4646903 (CYP1A1 MspI polymorphism) are significantly associated with an increased risk of CAD with respective odds ratios of 1.53703, 1.67710, and 1.35520; the genetic variant rs9579646 (ALOX5AP) is significantly associated with a decreased risk of CAD (OR 0.76163). Moreover, a significant smoking-gene interaction is determined with CYP1A1 MspI polymorphism rs4646903 and is associated with a decreased risk of CAD in current smokers (OR 0.52137). Conclusion This study provides further evidence that genetic variation of the LT pathway, PON1, and CYP1A1 can modulate the atherogenic processes and eventually increase the risk of CAD in our study population. Moreover, it also shows the effect of smoking-gene interaction on CAD risk, where the CYP1A1 MspI polymorphism revealed a decreased risk in current smokers. |
| eu_rights_str_mv | openAccess |
| format | article |
| id | LAURepo_fdfd13eeb38c4c32c3e7e25e24af34ef |
| identifier_str_mv | 1023-3830 Merhi, M., Demirdjian, S., Hariri, E., Sabbah, N., Youhanna, S., Ghassibe-Sabbagh, M., ... & Chammas, E. (2015). Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk. Inflammation Research, 64(6), 415-422. |
| language_invalid_str_mv | en |
| network_acronym_str | LAURepo |
| network_name_str | Lebanese American University repository |
| oai_identifier_str | oai:laur.lau.edu.lb:10725/3347 |
| publishDate | 2015 |
| repository.mail.fl_str_mv | |
| repository.name.fl_str_mv | |
| repository_id_str | |
| spelling | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease riskMerhi, MahmoudDemirdjian, SallyHariri, EssaSabbah, NadaYouhanna, SoniaGhassibe-Sabbagh, MichellaNaoum, JosephHaber, MarcKanbar, RoyZalloua, PierreKhazen, GeorgesBackground The role of inflammation in coronary artery disease (CAD) pathogenesis is well recognized. Moreover, smoking inhalation increases the activity of inflammatory mediators through an increase in leukotriene synthesis essential in atherosclerosis pathogenesis. Aim The aim of this study is to investigate the effect of “selected” genetic variants within the leukotriene (LT) pathway and other variants on the development of CAD. Methods CAD was detected by cardiac catheterization. Logistic regression was performed to investigate the association of smoking and selected susceptibility variants in the LT pathway including ALOX5AP, LTA4H, LTC4S, PON1, and LTA as well as CYP1A1 on CAD risk while controlling for age, gender, BMI, family history, diabetes, hyperlipidemia, and hypertension. Results rs4769874 (ALOX5AP), rs854560 (PON1), and rs4646903 (CYP1A1 MspI polymorphism) are significantly associated with an increased risk of CAD with respective odds ratios of 1.53703, 1.67710, and 1.35520; the genetic variant rs9579646 (ALOX5AP) is significantly associated with a decreased risk of CAD (OR 0.76163). Moreover, a significant smoking-gene interaction is determined with CYP1A1 MspI polymorphism rs4646903 and is associated with a decreased risk of CAD in current smokers (OR 0.52137). Conclusion This study provides further evidence that genetic variation of the LT pathway, PON1, and CYP1A1 can modulate the atherogenic processes and eventually increase the risk of CAD in our study population. Moreover, it also shows the effect of smoking-gene interaction on CAD risk, where the CYP1A1 MspI polymorphism revealed a decreased risk in current smokers.PublishedN/A2016-03-17T09:19:37Z2016-03-17T09:19:37Z20152016-03-17Articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1023-3830http://hdl.handle.net/10725/3347http://dx.doi.org/10.1007/s00011-015-0821-1Merhi, M., Demirdjian, S., Hariri, E., Sabbah, N., Youhanna, S., Ghassibe-Sabbagh, M., ... & Chammas, E. (2015). Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk. Inflammation Research, 64(6), 415-422.http://link.springer.com/article/10.1007/s00011-015-0821-1enInflammation Researchinfo:eu-repo/semantics/openAccessoai:laur.lau.edu.lb:10725/33472020-02-20T11:07:41Z |
| spellingShingle | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk Merhi, Mahmoud |
| status_str | publishedVersion |
| title | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| title_full | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| title_fullStr | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| title_full_unstemmed | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| title_short | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| title_sort | Impact of inflammation, gene variants, and cigarette smoking on coronary artery disease risk |
| url | http://hdl.handle.net/10725/3347 http://dx.doi.org/10.1007/s00011-015-0821-1 http://link.springer.com/article/10.1007/s00011-015-0821-1 |