Evidence map›Paper›PMID 27273790›Full record

ReviewBritish journal of pharmacology2017

Therapeutic potential of NADPH oxidase 1/4 inhibitors.

G Teixeira, C Szyndralewiez, S Molango, S Carnesecchi, F Heitz, P Wiesel, J M Wood

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
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  7. AβInternational journal of molecular sciences · 2025
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14 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 2 countries.

G TeixeiraEvotec International GmbH, Goettingen, Germany.
C SzyndralewiezGenkyotex SA, Plan les Ouates, Switzerland.
S MolangoGenkyotex SA, Plan les Ouates, Switzerland.
S CarnesecchiGenkyotex SA, Plan les Ouates, Switzerland.
F HeitzGenkyotex SA, Plan les Ouates, Switzerland.
P WieselGenkyotex SA, Plan les Ouates, Switzerland.
J M WoodInovaid, Biel-Benken, Switzerland.
Genkyotex (Switzerland) · CHEvotec (Germany) · DESpitalzentrum Centre hospitalier Biel- Bienne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NADPH oxidase (NOX) family of enzymes produces ROS as their sole function and is becoming recognized as key modulators of signal transduction pathways with a physiological role under acute stress and a pathological role after excessive activation under chronic stress. The seven isoforms differ in their regulation, tissue and subcellular localization and ROS products. The most studied are NOX1, 2 and 4. Genetic deletion of NOX1 and 4, in contrast to NOX2, has revealed no significant spontaneous pathologies and a pathogenic relevance of both NOX1 and 4 across multiple organs in a wide range of diseases and in particular inflammatory and fibrotic diseases. This has stimulated interest in NOX inhibitors for therapeutic application. GKT136901 and GKT137831 are two structurally related compounds demonstrating a preferential inhibition of NOX1 and 4 that have suitable properties for in vivo studies and have consequently been evaluated across a range of disease models and compared with gene deletion. In contrast to gene deletion, these inhibitors do not completely suppress ROS production, maintaining some basal level of ROS. Despite this and consistent with most gene deletion studies, these inhibitors are well tolerated and slow or prevent disease progression in a range of models of chronic inflammatory and fibrotic diseases by modulating common signal transduction pathways. Clinical trials in patients with GKT137831 have demonstrated excellent tolerability and reduction of various markers of chronic inflammation. NOX1/4 inhibition may provide a safe and effective therapeutic strategy for a range of inflammatory and fibrotic diseases. LINKED ARTICLES: This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.

Indexed as

AnimalsAnti-Inflammatory AgentsEnzyme InhibitorsFibrosisHumansInflammationNADPH Oxidase 1NADPH Oxidase 2PyrazolesPyrazolonesPyridinesPyridones2-(2-chlorophenyl)-4-methyl-5-(pyridin-2-ylmethyl)-1H-pyrazolo(4,3-c)pyridine-3,6(2H,5H)-dioneAnti-Inflammatory AgentsEnzyme InhibitorsNADPH Oxidase 1NADPH Oxidase 2PyrazolesPyrazolonesPyridinesPyridonessetanaxib

Identifiers

PMID27273790
PMCPMC5446584
OpenAlexW2414686680

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.