Evidence map›Paper›PMID 20567875›Full record

ArticleClinical and experimental medicine2011

Plasminogen activator inhibitor-1 polymorphisms (-844 G>A and HindIII C>G) in systemic lupus erythematosus: association with clinical variables.

Jorge Ramón Padilla-Gutiérrez, Claudia Azucena Palafox-Sánchez, Yeminia Valle, Gerardo Orozco-Barocio, Edith Oregón-Romero, Mónica Vázquez-Del Mercado, Héctor Rangel-Villalobos, Mara Anaís Llamas-Covarrubias, José Francisco Muñoz-Valle

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Article in Clinical and experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 40% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 6 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Jorge Ramón Padilla-GutiérrezInstituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de Salud, Universidad de Guadalajara, Insurgentes 244-1, Colonia Lomas de Atemajac, 45178 Zapopan, Jalisco, México.
Claudia Azucena Palafox-Sánchez
Yeminia Valle
Gerardo Orozco-Barocio
Edith Oregón-Romero
Mónica Vázquez-Del Mercado
Héctor Rangel-Villalobos
Mara Anaís Llamas-Covarrubias
José Francisco Muñoz-Valle
Universidad de Guadalajara · MXSecretaría de Salud de Jalisco · MXUniversidad de la Ciénega · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of autoantibodies against nuclear autoantigens as well as cytoplasmic and circulating proteins. Recent studies have demonstrated mechanisms responsible for modulation of the immune response by the plasminogen activator inhibitor-1 (PAI-1). Furthermore, the endogenous PAI-1 has shown to promote a Th2 immune response. We assessed the -844 G>A and HindIII C>G PAI-1 polymorphisms in SLE. In a case-control study of 71 SLE patients classified according to ACR criteria and 71 healthy subjects (HS). The A allele of -844 PAI-1 polymorphism showed a significant difference in SLE patients (41%) when compared with HS (27%) [P = 0.01; OR = 1.8, 95%, CI = 1.1-3.0]. In addition, the -844 G>A PAI-1 polymorphism was associated with increased risk for SLE in a dominant genetic model (G/G vs. G/A + A/A; OR = 2.3, 95% CI = 1.14-4.44). Also, anti-RNP positive antibodies in SLE were associated with G/G -844 PAI-1 genotype. The HindIII polymorphism did not show any differences. The haplotype analysis showed that the AC haplotype confers susceptibility to SLE (OR = 3.1, 95% CI, 1.45-6.52; P = 0.003). The AC haplotype of the -844 and HindIII PAI-1 polymorphism might be an additional susceptibility factor to SLE in Mexicans.

Indexed as

Polymorphism, Single NucleotideAdolescentAdultAgedCase-Control StudiesFemaleGene FrequencyHumansLupus Erythematosus, SystemicMaleMexicoMiddle AgedPlasminogen Activator Inhibitor 1Young AdultPlasminogen Activator Inhibitor 1SERPINE1 protein, human

Identifiers

PMID20567875
OpenAlexW2067019312

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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.