Evidence map›Paper›PMID 22360682›Full record

ArticleDNA and cell biology2012

Lack of association between TLR4 rs4986790 polymorphism and risk of cardiovascular disease in patients with rheumatoid arthritis.

Mercedes García-Bermúdez, Raquel López-Mejías, Carlos González-Juanatey, Santos Castañeda, José A Miranda-Filloy, Ricardo Blanco, Benjamín Fernández-Gutiérrez, Alejandro Balsa, Isidoro González-Alvaro, Carmen Gómez-Vaquero and 3 more

Open access · greenAbstract read
In one paragraph

Article in DNA and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 7 institutions in 1 country.

Mercedes García-BermúdezInstituto de Parasitología y Biomedicina López-Neyra, IPBLN-CSIC, Granada, Spain.
Raquel López-Mejías
Carlos González-Juanatey
Santos Castañeda
José A Miranda-Filloy
Ricardo Blanco
Benjamín Fernández-Gutiérrez
Alejandro Balsa
Isidoro González-Alvaro
Carmen Gómez-Vaquero
Javier Llorca
Javier Martín
Miguel A González-Gay
Fundación Marques de Valdecilla · ESHospital Universitario de La Princesa · ESHospital Xeral Calde · ESInstituto de Parasitología y Biomedicina "López - Neyra" · ESHospital Clínico San Carlos · ESHospital Universitario La Paz · ESUniversidad de Cantabria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 mitogen-activated 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.

Indexed as

Polymorphism, Single NucleotideAdultArthritis, RheumatoidAtherosclerosisCardiovascular DiseasesFemaleGene FrequencyGenetic MarkersGenetic Predisposition to DiseaseHumansMaleMiddle AgedSignal TransductionToll-Like Receptor 4Genetic MarkersTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID22360682
PMCPMC3391495
OpenAlexW2023717707

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.