Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis

Cardiovascular (CV) disease is the most common cause of premature mortality in patients with rheumatoid arthritis (RA). It is the result of an accelerated atherosclerotic process. Both RA and atherosclerosis are complex polygenic diseases. Besides traditional CV risk factors and chronic inflammation...

Full description

Saved in:
Bibliographic Details
Main Authors: Luis Rodríguez-Rodríguez, Raquel López-Mejías, Mercedes García-Bermúdez, Carlos González-Juanatey, Miguel A. González-Gay, Javier Martín
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2012/574817
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832556209609113600
author Luis Rodríguez-Rodríguez
Raquel López-Mejías
Mercedes García-Bermúdez
Carlos González-Juanatey
Miguel A. González-Gay
Javier Martín
author_facet Luis Rodríguez-Rodríguez
Raquel López-Mejías
Mercedes García-Bermúdez
Carlos González-Juanatey
Miguel A. González-Gay
Javier Martín
author_sort Luis Rodríguez-Rodríguez
collection DOAJ
description Cardiovascular (CV) disease is the most common cause of premature mortality in patients with rheumatoid arthritis (RA). It is the result of an accelerated atherosclerotic process. Both RA and atherosclerosis are complex polygenic diseases. Besides traditional CV risk factors and chronic inflammation, a number of studies have confirmed the role of genetic factors in the development of the atherogenesis observed in RA. In this regard, besides a strong association between the HLA-DRB1*04 shared epitope alleles and both endothelial dysfunction, an early step in the atherosclerotic process, and clinically evident CV disease, other polymorphisms belonging to genes implicated in inflammatory and metabolic pathways, located inside and outside the HLA region, such as the 308 variant (G>A, rs1800629) of the TNFA locus, the rs1801131 polymorphism (A>C; position + 1298) of the MTHFR locus, or a deletion of 32 base pairs on the CCR5 gene, seem to be associated with the risk of CV disease in patients with RA. Despite considerable effort to decipher the genetic basis of CV disease in RA, further studies are required to better establish the genetic influence in the increased risk of CV events observed in patients with RA.
format Article
id doaj-art-a77408d1b72d4f74a893b4a212f933b3
institution Kabale University
issn 0962-9351
1466-1861
language English
publishDate 2012-01-01
publisher Wiley
record_format Article
series Mediators of Inflammation
spelling doaj-art-a77408d1b72d4f74a893b4a212f933b32025-02-03T05:46:08ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/574817574817Genetic Markers of Cardiovascular Disease in Rheumatoid ArthritisLuis Rodríguez-Rodríguez0Raquel López-Mejías1Mercedes García-Bermúdez2Carlos González-Juanatey3Miguel A. González-Gay4Javier Martín5Department of Rheumatology, Hospital Clínico San Carlos, c/Profesor Martín Lagos s/n, 28040 Madrid, SpainDepartment of Rheumatology, Hospital Universitario Marqués de Valdecilla, IFIMAV, Avenida Herrera Oria s/n, 39011 Santander, SpainInstituto de Parasitología y Biomedicina López-Neyra, CSIC, Parque Tecnológico de Ciencias de la Salud, Avenida del Conocimiento s/n, Armilla, 18100 Granada, SpainCardiology Division, Hospital Xeral-Calde, c/Dr. Ochoa s/n, 27004 Lugo, SpainDepartment of Rheumatology, Hospital Universitario Marqués de Valdecilla, IFIMAV, Avenida Herrera Oria s/n, 39011 Santander, SpainInstituto de Parasitología y Biomedicina López-Neyra, CSIC, Parque Tecnológico de Ciencias de la Salud, Avenida del Conocimiento s/n, Armilla, 18100 Granada, SpainCardiovascular (CV) disease is the most common cause of premature mortality in patients with rheumatoid arthritis (RA). It is the result of an accelerated atherosclerotic process. Both RA and atherosclerosis are complex polygenic diseases. Besides traditional CV risk factors and chronic inflammation, a number of studies have confirmed the role of genetic factors in the development of the atherogenesis observed in RA. In this regard, besides a strong association between the HLA-DRB1*04 shared epitope alleles and both endothelial dysfunction, an early step in the atherosclerotic process, and clinically evident CV disease, other polymorphisms belonging to genes implicated in inflammatory and metabolic pathways, located inside and outside the HLA region, such as the 308 variant (G>A, rs1800629) of the TNFA locus, the rs1801131 polymorphism (A>C; position + 1298) of the MTHFR locus, or a deletion of 32 base pairs on the CCR5 gene, seem to be associated with the risk of CV disease in patients with RA. Despite considerable effort to decipher the genetic basis of CV disease in RA, further studies are required to better establish the genetic influence in the increased risk of CV events observed in patients with RA.http://dx.doi.org/10.1155/2012/574817
spellingShingle Luis Rodríguez-Rodríguez
Raquel López-Mejías
Mercedes García-Bermúdez
Carlos González-Juanatey
Miguel A. González-Gay
Javier Martín
Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis
Mediators of Inflammation
title Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis
title_full Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis
title_fullStr Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis
title_full_unstemmed Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis
title_short Genetic Markers of Cardiovascular Disease in Rheumatoid Arthritis
title_sort genetic markers of cardiovascular disease in rheumatoid arthritis
url http://dx.doi.org/10.1155/2012/574817
work_keys_str_mv AT luisrodriguezrodriguez geneticmarkersofcardiovasculardiseaseinrheumatoidarthritis
AT raquellopezmejias geneticmarkersofcardiovasculardiseaseinrheumatoidarthritis
AT mercedesgarciabermudez geneticmarkersofcardiovasculardiseaseinrheumatoidarthritis
AT carlosgonzalezjuanatey geneticmarkersofcardiovasculardiseaseinrheumatoidarthritis
AT miguelagonzalezgay geneticmarkersofcardiovasculardiseaseinrheumatoidarthritis
AT javiermartin geneticmarkersofcardiovasculardiseaseinrheumatoidarthritis