Lack of association between TLR4 rs4986790 polymorphism and risk of cardiovascular disease in patients with rheumatoid arthritis
Autor (es)
García-Bermúdez, Mercedes; López-Mejías, Raquel; González-Juanatey, Carlos; Castañeda Sanz, Santos; Miranda-Filloy, José Alberto; Blanco, Ricardo; Fernández-Gutiérrez, Benjamín; Balsa Criado, Alejandro; González-álvaro, Isidoro; Gómez-Vaquero, Carmen; Llorca, Javier; Martín, Javier E.; González-Gay, Miguel ÁngelEditor
Mary Ann Liebert, Inc.Fecha de edición
2012-07-01Cita
10.1089/dna.2011.1582
DNA and cell biology 31.7 (2012): 1214-1220
ISSN
1044-5498 (print); 1557-7430 (online)DOI
10.1089/dna.2011.1582Financiado por
This study was supported by two grants from Fondo de Investigaciones Sanitarias PI06-0024 and PS09/00748 (Spain). This work was partially supported by RETICS Program, RD08/0075 (RIER) from Instituto de Salud Carlos III (ISCIII), within the VI PN de I +D+ i 2008–2011 (FEDER). M.G.B. is supported by a grant from Fundación Española de Reumatología (FER). R.L.M. is supported by a grant by IFIMAV, Santander (Spain).Versión del editor
http://dx.doi.org/10.1089/dna.2011.1582Materias
TLR4 rs4986790; Polymorphism; Risk of Cardiovascular Disease; Patients; Rheumatoid Arthritis; MedicinaNota
This is copy of an article published in the DNA and cell biology 2012 © Mary Ann Liebert, Inc.; DNA and cell bilogy is available online at: http://online.liebertpub.comDerechos
© Mary Ann Liebert, Inc.Resumen
Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with increased cardiovascular (CV)
mortality. Toll-like receptor-4 (TLR4) activates the innate immune response via NF-kB pathway and mitogenactivated
protein kinase signaling, leading to expression of proinflammatory cytokines and chemokines. The G
allele of TLR4 rs4986790 (+ 896A > G, Asp299Gly) gene polymorphism has been implicated in reduction of risk of
atherosclerosis. In this study, 1481 RA patients fulfilling the 1987 American College of Rheumatology (ACR)
criteria were genotyped for the rs4986790 TLR4 variant to determine the influence of this variant in the risk of CV
events in these patients. Also, HLA-DRB1 status was determined using molecular based methods. Moreover,
potential influence of rs4986790 variant in the development of subclinical atherosclerosis was assessed in a
subgroup of RA patients with no history of CV events by the measurement of surrogate markers of subclinical
atherosclerosis. No statistically significant differences in allele or genotype frequencies for the rs4986790 variant
between RA patients who experienced CV events or not were found. Likewise, no significant association between
this gene variant and any of the surrogate markers of subclinical atherosclerosis was found. In summary,
results in our study do not support the hypothesis that the rs4986790 (+ 896A > G, Asp299Gly) TLR4 variant may
influence predisposition for subclinical atherosclerosis and clinically evident CV disease in RA patients
Lista de ficheros
Google Scholar:García-Bermúdez, Mercedes
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López-Mejías, Raquel
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González-Juanatey, Carlos
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Castañeda Sanz, Santos
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Miranda-Filloy, José Alberto
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Blanco, Ricardo
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Fernández-Gutiérrez, Benjamín
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Balsa Criado, Alejandro
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González-álvaro, Isidoro
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Gómez-Vaquero, Carmen
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Llorca, Javier
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Martín, Javier E.
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González-Gay, Miguel Ángel
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