Evidence map›Paper›PMID 29571125›Full record

ReviewRedox biology2018

NADPH oxidases in traumatic brain injury - Promising therapeutic targets?

Merry W Ma, Jing Wang, Krishnan M Dhandapani, Ruimin Wang, Darrell W Brann

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
7.0field-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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  10. Review
  11. Article
  12. Delayed COCNS neuroscience & therapeutics · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Amplified Gliosis and Interferon-Associated Inflammation in the Aging Brain following Diffuse Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  19. Article
  20. NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022
    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

5 authors at 2 institutions in 2 countries.

Merry W MaDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Jing WangDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Krishnan M DhandapaniDepartment of Neurosurgery, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Ruimin WangDepartment of Neurobiology, North China University of Science and Technology, Tangshan, Hebei, China.
Darrell W BrannDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA. Electronic address: dbrann@augusta.edu.
Augusta University · USNorth China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Despite intense investigation, no neuroprotective agents for TBI have yet translated to the clinic. Recent efforts have focused on identifying potential therapeutic targets that underlie the secondary TBI pathology that evolves minutes to years following the initial injury. Oxidative stress is a key player in this complex cascade of secondary injury mechanisms and prominently contributes to neurodegeneration and neuroinflammation. NADPH oxidase (NOX) is a family of enzymes whose unique function is to produce reactive oxygen species (ROS). Human post-mortem and animal studies have identified elevated NOX2 and NOX4 levels in the injured brain, suggesting that these two NOXs are involved in the pathogenesis of TBI. In support of this, NOX2 and NOX4 deletion studies have collectively revealed that targeting NOX enzymes can reduce oxidative stress, attenuate neuroinflammation, promote neuronal survival, and improve functional outcomes following TBI. In addition, NOX inhibitor studies have confirmed these findings and demonstrated an extended critical window of efficacious TBI treatment. Finally, the translational potential, caveats, and future directions of the field are highlighted and discussed throughout the review.

Indexed as

BrainBrain Injuries, TraumaticHumansNADPH Oxidase 2NADPH Oxidase 4NADPH OxidasesNeuronsOxidation-ReductionOxidative StressReactive Oxygen SpeciesCYBB protein, humanNADPH Oxidase 2NADPH Oxidase 4NADPH OxidasesNOX4 protein, humanReactive Oxygen SpeciesApocyninCCICHIControlled cortical impactFPIgp91ds-tatMicrogliaNADPH oxidaseNOXNOX1NOX2NOX4Oxidative stressROSTBITraumatic brain injury

Identifiers

PMID29571125
PMCPMC5952873
OpenAlexW2792862972

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.