Evidence map›Paper›PMID 30897521›Full record

ArticleRedox biology2019

NADPH oxidase 2 inhibitors CPP11G and CPP11H attenuate endothelial cell inflammation & vessel dysfunction and restore mouse hind-limb flow.

Y Li, E Cifuentes-Pagano, E R DeVallance, D S de Jesus, S Sahoo, D N Meijles, D Koes, C J Camacho, M Ross, C St Croix and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  9. Increased Neutrophil HResearch square · 2024
    Article
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  13. Article
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  15. Article
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  17. NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022
    Review
  18. Article
  19. Article
  20. 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

11 authors at 3 institutions in 1 country.

Y LiVascular Medicine Institute, USA; Department of Pharmacology & Chemical Biology, USA.
E Cifuentes-PaganoVascular Medicine Institute, USA; Department of Pharmacology & Chemical Biology, USA.
E R DeVallanceVascular Medicine Institute, USA; Department of Pharmacology & Chemical Biology, USA.
D S de JesusVascular Medicine Institute, USA; Department of Pharmacology & Chemical Biology, USA.
S SahooVascular Medicine Institute, USA; Department of Pharmacology & Chemical Biology, USA.
D N MeijlesVascular Medicine Institute, USA.
D KoesComputational and Systems Biology, University of Pittsburgh, USA.
C J CamachoComputational and Systems Biology, University of Pittsburgh, USA.
M RossCenter for Biologic Imaging, University of Pittsburgh, PA, 15261, USA.
C St CroixCenter for Biologic Imaging, University of Pittsburgh, PA, 15261, USA.
P J PaganoVascular Medicine Institute, USA; Department of Pharmacology & Chemical Biology, USA. Electronic address: pagano@pitt.edu.
Reproductive Medicine Institute · USUniversity of Pittsburgh · USDivision of Chemistry · US

Funding

Vascular Subphenotypes of Lung DiseaseP01HL103455 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2011 to 2020
$26.1M
Translational Pulmonary Vascular BiologyT32HL110849 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sruti Shiva · 2012 to 2026
$5.0M
Reactive Oxygen Species in Vascular DiseaseR01HL079207 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PAGANO, PATRICK J · 2007 to 2018
$3.4M
Real-time discovery of inhibitors among billion compounds for preview and downloadR01GM097082 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CAMACHO, CARLOS J. · 2011 to 2020
$2.5M
Progressive degenerative role of Nox and thrombospondin-1 in the aging vasculatureR01HL142248 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PAGANO, PATRICK J · 2019 to 2022
$2.3M
NHLBI NIH HHS P01 HL103455NHLBI NIH HHS R01 HL079207NHLBI NIH HHS R01 HL142248NHLBI NIH HHS T32 HL110849NIGMS NIH HHS R01 GM097082
6 · The paper itself

Abstract

First described as essential to the phagocytic activity of leukocytes, Nox2-derived ROS have emerged as mediators of a range of cellular and tissue responses across species from salubrious to deleterious consequences. Knowledge of their role in inflammation is limited, however. We postulated that TNFα-induced endothelial reactive oxygen species (ROS) generation and pro-inflammatory signaling would be ameliorated by targeting Nox2. Herein, we in silico-modelled two first-in-class Nox2 inhibitors developed in our laboratory, explored their cellular mechanism of action and tested their efficacy in in vitro and mouse in vivo models of inflammation. Our data show that these inhibitors (CPP11G and CPP11H) disrupted canonical Nox2 organizing factor, p47

Indexed as

AnimalsBiomarkersCell AdhesionCell LineEndothelial CellsEnzyme InhibitorsHindlimbHumansMiceModels, MolecularMolecular ConformationMonocytesNADPH Oxidase 2NF-kappa BProtein BindingProtein Interaction Domains and MotifsBiomarkersEnzyme InhibitorsNADPH Oxidase 2NF-kappa BReactive Oxygen SpeciesTranscription Factor AP-1Endothelial dysfunctionNADPH oxidaseReactive oxygen speciesSmall-molecule inhibitorVascular inflammation

Identifiers

PMID30897521
PMCPMC6435978
OpenAlexW2913499353

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.