Evidence map›Paper›PMID 28095923›Full record

ReviewMolecular neurodegeneration2017

NADPH oxidase in brain injury and neurodegenerative disorders.

Merry W Ma, Jing Wang, Quanguang Zhang, Ruimin Wang, Krishnan M Dhandapani, Ratna K Vadlamudi, Darrell W Brann

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
246citing papers in PubMed, 1 pooled it
17.2field-weighted citation impact, top 1% 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

246 citing papers in PubMed, 1 synthesis or guideline pooled it, 418 citations in OpenAlex.

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  12. Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026
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186 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 1 country.

Merry W MaCharlie Norwood VA Medical Center, One Freedom Way, Augusta, GA, 30904, USA.
Jing WangCharlie Norwood VA Medical Center, One Freedom Way, Augusta, GA, 30904, USA.
Quanguang ZhangCharlie Norwood VA Medical Center, One Freedom Way, Augusta, GA, 30904, USA.
Ruimin WangCharlie Norwood VA Medical Center, One Freedom Way, Augusta, GA, 30904, USA.
Krishnan M DhandapaniCharlie Norwood VA Medical Center, One Freedom Way, Augusta, GA, 30904, USA.
Ratna K VadlamudiDepartment of Obstetrics and Gynecology, University of Texas Health Science Center, 7703 Medical Drive, San Antonio, TX, 78229, USA.
Darrell W BrannCharlie Norwood VA Medical Center, One Freedom Way, Augusta, GA, 30904, USA. dbrann@augusta.edu.
Charlie Norwood VA Medical Center · USAugusta University · USThe University of Texas Health Science Center at San Antonio · US

Funding

Neuroprotective and Neurogenic Actions of E2 and SERMsR01NS050730 · NINDS · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BRANN, DARRELL W, VADLAMUDI, RATNA K · 2005 to 2014
$3.2M
Brain Aromatase in Neurological Function and DiseaseR01NS088058 · NINDS · AUGUSTA UNIVERSITY · PI BRANN, DARRELL W, VADLAMUDI, RATNA K · 2015 to 2019
$1.8M
NINDS NIH HHS R01 NS050730NINDS NIH HHS R01 NS088058
6 · The paper itself

Abstract

Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.

Indexed as

AnimalsBrain InjuriesHumansNADPH OxidasesNeurodegenerative DiseasesNADPH OxidasesAlzheimer’s diseaseAmyotrophic lateral sclerosisHuntington’s diseaseMultiple sclerosisNADPH oxidaseNeurodegenerationOxidative stressParkinson’s diseaseStrokeTraumatic brain injury

Identifiers

PMID28095923
PMCPMC5240251
OpenAlexW2574254633

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.