Evidence map›Paper›PMID 27540362›Full record

ArticleFrontiers in pharmacology2016

Detoxifying Enzymes at the Cross-Roads of Inflammation, Oxidative Stress, and Drug Hypersensitivity: Role of Glutathione Transferase P1-1 and Aldose Reductase.

Francisco J Sánchez-Gómez, Beatriz Díez-Dacal, Elena García-Martín, José A G Agúndez, María A Pajares, Dolores Pérez-Sala

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  4. Protein Haptenation and Its Role in Allergy.Chemical research in toxicology · 2024
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  11. Review
  12. Lack of Major Involvement of CommonFrontiers in pharmacology · 2021
    Article
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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

6 authors at 3 institutions in 1 country.

Francisco J Sánchez-GómezDepartment of Chemical and Physical Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas Madrid, Spain.
Beatriz Díez-DacalDepartment of Chemical and Physical Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas Madrid, Spain.
Elena García-MartínDepartment of Pharmacology, University of Extremadura Cáceres, Spain.
José A G AgúndezDepartment of Pharmacology, University of Extremadura Cáceres, Spain.
María A PajaresInstituto de Investigaciones Biomédicas Alberto Sols (Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid), and Grupo de Hepatología Molecular, Instituto de Investigación Sanitaria del Hospital Universitario La Paz (IdiPAZ) Madrid, Spain.
Dolores Pérez-SalaDepartment of Chemical and Physical Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas Madrid, Spain.
Centro de Investigaciones Biológicas Margarita Salas · ESConsejo Superior de Investigaciones Científicas · ESUniversidad de Extremadura · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phase I and II enzymes are involved in the metabolism of endogenous reactive compounds as well as xenobiotics, including toxicants and drugs. Genotyping studies have established several drug metabolizing enzymes as markers for risk of drug hypersensitivity. However, other candidates are emerging that are involved in drug metabolism but also in the generation of danger or costimulatory signals. Enzymes such as aldo-keto reductases (AKR) and glutathione transferases (GST) metabolize prostaglandins and reactive aldehydes with proinflammatory activity, as well as drugs and/or their reactive metabolites. In addition, their metabolic activity can have important consequences for the cellular redox status, and impacts the inflammatory response as well as the balance of inflammatory mediators, which can modulate epigenetic factors and cooperate or interfere with drug-adduct formation. These enzymes are, in turn, targets for covalent modification and regulation by oxidative stress, inflammatory mediators, and drugs. Therefore, they constitute a platform for a complex set of interactions involving drug metabolism, protein haptenation, modulation of the inflammatory response, and/or generation of danger signals with implications in drug hypersensitivity reactions. Moreover, increasing evidence supports their involvement in allergic processes. Here, we will focus on GSTP1-1 and aldose reductase (AKR1B1) and provide a perspective for their involvement in drug hypersensitivity.

Indexed as

aldose reductaseallergydetoxificationdrug adductdrug hypersensitivityglutathione transferaseinflammationoxidative stress

Identifiers

PMID27540362
PMCPMC4973429
OpenAlexW2491134085

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.