Evidence map›Paper›PMID 35740890›Full record

ArticleBiomolecules2022

Gilberto Vargas-Alarcón, Julian Ramírez-Bello, Marco Antonio Peña-Duque, Marco Antonio Martínez-Ríos, Hilda Delgadillo-Rodríguez, José Manuel Fragoso

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
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

6 authors at 1 institution in 1 country.

Gilberto Vargas-AlarcónDepartment of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.
Julian Ramírez-BelloDepartment of Endocrinology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.ORCID 0000-0002-4153-9315
Marco Antonio Peña-DuqueDepartment of Innovation and Technological Development, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.
Marco Antonio Martínez-RíosDepartment of Hemodynamics, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.
Hilda Delgadillo-RodríguezDepartment of Hemodynamics, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.
José Manuel FragosoDepartment of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.ORCID 0000-0003-3137-7815
Instituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study, we evaluated the association of the BAT1, NFKBIL, LTA, and CASP1 single nucleotide polymorphisms and the gene−gene interactions with risk of developing restenosis after coronary stenting. The allele and genotype determination of the polymorphisms (BAT1 rs2239527 C/G, NFKBIL1 rs2071592 T/A, LTA rs1800683 G/A, CASP1 rs501192 A/G, and CASP1 rs580253 A/G) were performed by 5’exonuclease TaqMan assays in 219 patients: 66 patients with restenosis and 153 without restenosis. The distribution of rs2239527 C/G, rs2071592 T/A, and rs1800683 G/A polymorphisms was similar in patients with and without restenosis. Nonetheless, under recessive (OR = 2.73, pCRes = 0.031) and additive models (OR = 1.65, pCAdd = 0.039), the AA genotype of the rs501192 A/G polymorphism increased the restenosis risk. Under co-dominant, dominant, recessive, and additive models, the AA genotype of the rs580253 A/G was associated with a high restenosis risk (OR = 5.38, pCCo-Dom = 0.003; OR = 2.12, pCDom = 0.031; OR = 4.32, pCRes = 0.001; and OR = 2.16, 95%CI: 1.33−3.52, pCAdd = 0.001, respectively). In addition, we identified an interaction associated with restenosis susceptibility: BAT1-NFKBIL1-LTA-CASP1 (OR = 9.92, p < 0.001). In summary, our findings demonstrate that the rs501192 A/G and rs580253 A/G polymorphisms, as well as the gene−gene interactions between BAT1-NFKBIL1-LTA-CASP1, are associated with an increased restenosis risk after coronary stenting.

Indexed as

Caspase 1Coronary RestenosisGenetic Predisposition to DiseaseAllelesEpistasis, GeneticHumansPolymorphism, Single NucleotideCaspase 1geneticspolymorphismsrestenosissusceptibility

Identifiers

PMID35740890
PMCPMC9221501
OpenAlexW4281694692

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.