Evidence map›Paper›PMID 32647953›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2020

Genetic contribution of endoplasmic reticulum aminopeptidase 1 polymorphisms to liver fibrosis progression in patients with HCV infection.

Jose Ramón Vidal-Castiñeira, Antonio López-Vázquez, Paula Diaz-Bulnes, Susana Díaz-Coto, Leonardo Márquez-Kisinousky, Jesús Martínez-Borra, Carmen A Navascues, Paloma Sanz-Cameno, Juan de la Vega, Aurora Astudillo and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

12 authors at 5 institutions in 1 country.

Jose Ramón Vidal-CastiñeiraTranslational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), Hospital Universitario Central de Asturias, Oviedo, Spain.ORCID 0000-0003-4877-3566
Antonio López-VázquezTranslational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), Hospital Universitario Central de Asturias, Oviedo, Spain.
Paula Diaz-BulnesTranslational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), Hospital Universitario Central de Asturias, Oviedo, Spain.
Susana Díaz-CotoStatistical Department, Universidad de Oviedo, Oviedo, Spain.
Leonardo Márquez-KisinouskyTranslational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), Hospital Universitario Central de Asturias, Oviedo, Spain.
Jesús Martínez-BorraTranslational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), Hospital Universitario Central de Asturias, Oviedo, Spain.
Carmen A NavascuesGastroenterology Service, Hospital Universitario Central de Asturias, Oviedo, Spain.
Paloma Sanz-CamenoLiver Unit, Gastroenterology Service, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa (IIS-IP), Universidad Autónoma de Madrid and CIBERehd, Instituto de Salud Carlos III, Madrid, Spain.
Juan de la VegaGastroenterology Service, Hospital San Agustín, Avilés, Spain.
Aurora AstudilloPathology Service, Hospital Universitario Central de Asturias, Oviedo, Spain.
Manuel RodríguezGastroenterology Service, Hospital Universitario Central de Asturias, Oviedo, Spain.
Carlos López-LarreaTranslational Immunology Laboratory, Health Research Institute of the Principality of Asturias (ISPA), Hospital Universitario Central de Asturias, Oviedo, Spain. inmuno@hca.es.
Hospital Universitario Central de Asturias · ESInstituto de Investigación Sanitaria del Principado de Asturias · ESHospital Universitario San Agustín · ESInstituto de Salud Carlos III · ESUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The endoplasmic reticulum aminopeptidase ERAP1 regulates innate and adaptive immune responses, trimming peptides and loading onto HLA class I molecules. Coding single nucleotide polymorphisms within ERAP1 are associated with autoimmune diseases, viral infections, and cancer development. Our purpose was to analyze the influence of ERAP1 variants on fibrogenesis in hepatitis C virus (HCV)-infected patients. A range of ERAP1 polymorphisms were genotyped in 722 unrelated Caucasian patients diagnosed with chronic HCV from two Spanish cohorts. Patients were classified according to their fibrosis stage. Paraffin-embedded tissue microarrays were constructed to assess ERAP1 expression (HCV = 38; alcoholic = 20) by immunohistochemistry. A statistical algorithm was applied to derive a fibrogenesis prediction model. The ERAP1 variants rs30187/T (K528, p

Indexed as

HepacivirusPolymorphism, GeneticAllelesAminopeptidasesBiomarkersDisease SusceptibilityEndoplasmic ReticulumGenetic Predisposition to DiseaseGenotypeHepatitis CHumansLiver CirrhosisMinor Histocompatibility AntigensPhenotypePolymorphism, Single NucleotideTissue Array AnalysisAminopeptidasesBiomarkersERAP1 protein, humanMinor Histocompatibility AntigensEndoplasmic reticulum aminopeptidase-1Fibrosis developmentHepatitis C virusImmune modulatorsPolymorphisms

Identifiers

PMID32647953
OpenAlexW3041729170

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.