Evidence map›Paper›PMID 31852525›Full record

ArticleBMC pharmacology & toxicology2019

Nuclear factor erythroid 2 - related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis.

Luisa Jiménez-Vidal, Pedro Espitia-Pérez, José Torres-Ávila, Dina Ricardo-Caldera, Shirley Salcedo-Arteaga, Claudia Galeano-Páez, Karina Pastor-Sierra, Lyda Espitia-Pérez

Abstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2019. 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
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. The Role of Toxic Metals and Metalloids in Nrf2 Signaling.Antioxidants (Basel, Switzerland) · 2021
    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

8 authors.

Luisa Jiménez-VidalFacultad de Ciencias de la Salud, Grupo de Investigación Biomédica y Biología Molecular, Universidad del Sinú, Calle 38 Cra 1W, Barrio Juan XXIII, Montería, Córdoba, Colombia.
Pedro Espitia-PérezFacultad de Ciencias de la Salud, Grupo de Investigación Biomédica y Biología Molecular, Universidad del Sinú, Calle 38 Cra 1W, Barrio Juan XXIII, Montería, Córdoba, Colombia.
José Torres-ÁvilaUnit for Development and Innovation in Genetics and Molecular Biology, Universidad Simón Bolívar, Barranquilla, Atlántico, Colombia.
Dina Ricardo-CalderaFacultad de Ciencias de la Salud, Grupo de Investigación en Enfermedades Tropicales y Resistencia Bacteriana, Universidad del Sinú, Montería, Córdoba, Colombia.
Shirley Salcedo-ArteagaFacultad de Ciencias de la Salud, Grupo de Investigación Biomédica y Biología Molecular, Universidad del Sinú, Calle 38 Cra 1W, Barrio Juan XXIII, Montería, Córdoba, Colombia.
Claudia Galeano-PáezFacultad de Ciencias de la Salud, Grupo de Investigación Biomédica y Biología Molecular, Universidad del Sinú, Calle 38 Cra 1W, Barrio Juan XXIII, Montería, Córdoba, Colombia.
Karina Pastor-SierraFacultad de Ciencias de la Salud, Grupo de Investigación Biomédica y Biología Molecular, Universidad del Sinú, Calle 38 Cra 1W, Barrio Juan XXIII, Montería, Córdoba, Colombia.
Lyda Espitia-PérezFacultad de Ciencias de la Salud, Grupo de Investigación Biomédica y Biología Molecular, Universidad del Sinú, Calle 38 Cra 1W, Barrio Juan XXIII, Montería, Córdoba, Colombia. lydaespitia@unisinu.edu.co.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNickel and nickel-containing compounds (NCC) are known human carcinogens. However, the precise molecular mechanisms of nickel-induced malignant transformation remain unknown. Proposed mechanisms suggest that nickel and NCC may participate in the dual activation/inactivation of enzymatic pathways involved in cell defenses against oxidative damage, where Nuclear factor-erythroid 2 related factor 2 (Nrf2) plays a central role.

methodsFor assessing the potential role of proteins involved in the Nrf2-mediated response to nickel and NCC exposure, we designed an interactome network using the STITCH search engine version 5.0 and the STRING software 10.0. The major NCC-protein interactome (NCPI) generated was analyzed using the MCODE plugin, version 1.5.1 for the detection of interaction modules or subnetworks. Main centralities of the NCPI were determined with the CentiScape 2.2 plugin of Cytoscape 3.4.0 and main biological processes associated with each cluster were assessed using the BiNGO plugin of Cytoscape 3.4.0.

resultsWater-soluble NiSO

conclusionsCellular response to NCC exposure was very comparable, particularly concerning oxidative stress response, inflammation, cell cycle/proliferation, and apoptosis. In this cellular response, Nfr2 was highly centralized and participated in several multifunctional protein complexes, including several related to ER-stress. These results add evidence on the possible Ni

Indexed as

AnimalsCluster AnalysisEndoplasmic Reticulum StressHumansNF-E2-Related Factor 2NickelOxidative StressSolubilitySystems BiologyUnfolded Protein ResponseNFE2L2 protein, humanNF-E2-Related Factor 2Nickelnickel subsulfidenickel sulfateER-stressNi3S2NickelNiSO4Nrf2UPR

Identifiers

PMID31852525
PMCPMC6921378

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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.