Evidence map›Paper›PMID 24635113›Full record

ReviewAntioxidants & redox signaling2015

Pathophysiology and Treatments of Oxidative Injury in Ischemic Stroke: Focus on the Phagocytic NADPH Oxidase 2.

Federico Carbone, Priscila Camillo Teixeira, Vincent Braunersreuther, François Mach, Nicolas Vuilleumier, Fabrizio Montecucco

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 64 citations in OpenAlex.

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  12. NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022
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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 2 institutions in 3 countries.

Federico Carbone1 Division of Cardiology, Foundation for Medical Researches, Department of Medical Specialties, University of Geneva , Geneva, Switzerland .
Priscila Camillo Teixeira3 Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals , Geneva, Switzerland .
Vincent Braunersreuther1 Division of Cardiology, Foundation for Medical Researches, Department of Medical Specialties, University of Geneva , Geneva, Switzerland .
François Mach1 Division of Cardiology, Foundation for Medical Researches, Department of Medical Specialties, University of Geneva , Geneva, Switzerland .
Nicolas Vuilleumier3 Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals , Geneva, Switzerland .
Fabrizio Montecucco1 Division of Cardiology, Foundation for Medical Researches, Department of Medical Specialties, University of Geneva , Geneva, Switzerland .
University of Geneva · CHUniversity Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

significancePhagocytes play a key role in promoting the oxidative stress after ischemic stroke occurrence. The phagocytic NADPH oxidase (NOX) 2 is a membrane-bound enzyme complex involved in the antimicrobial respiratory burst and free radical production in these cells. RECENT ADVANCES: Different oxidants have been shown to induce opposite effects on neuronal homeostasis after a stroke. However, several experimental models support the detrimental effects of NOX activity (especially the phagocytic isoform) on brain recovery after stroke. Therapeutic strategies selectively targeting the neurotoxic ROS and increasing neuroprotective oxidants have recently produced promising results. CRITICAL ISSUES: NOX2 might promote carotid plaque rupture and stroke occurrence. In addition, NOX2-derived reactive oxygen species (ROS) released by resident and recruited phagocytes enhance cerebral ischemic injury, activating the inflammatory apoptotic pathways. The aim of this review is to update evidence on phagocyte-related oxidative stress, focusing on the role of NOX2 as a potential therapeutic target to reduce ROS-related cerebral injury after stroke. FUTURE DIRECTIONS: Radical scavenger compounds (such as Ebselen and Edaravone) are under clinical investigation as a therapeutic approach against stroke. On the other hand, NOX inhibition might represent a promising strategy to prevent the stroke-related injury. Although selective NOX inhibitors are not yet available, nonselective compounds (such as apocynin and fasudil) provided encouraging results in preclinical studies. Whereas additional studies are needed to better evaluate this therapeutic potential in human beings, the development of specific NOX inhibitors (such as monoclonal antibodies, small-molecule inhibitors, or aptamers) might further improve brain recovery after stroke.

Indexed as

AnimalsAntioxidantsAntipyrineAzolesBrainEdaravoneHumansIsoindolesMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesOrganoselenium CompoundsOxidation-ReductionOxidative StressPhagocytosisReactive Oxygen SpeciesAntioxidantsAntipyrineAzolesCYBB protein, humanebselenEdaravoneIsoindolesMembrane GlycoproteinsNADPH Oxidase 2NADPH OxidasesOrganoselenium CompoundsReactive Oxygen Species

Identifiers

PMID24635113
PMCPMC4545676
OpenAlexW2059014554

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.