Evidence map›Paper›PMID 30761998›Full record

ReviewNeural regeneration research2019

Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke.

Jiamei Shen, Radhika Rastogi, Xiaokun Geng, Yuchuan Ding

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The Role of NADPharmaceuticals (Basel, Switzerland) · 2024
    Review
  5. Cardioprotective Role ofCardiovascular & hematological agents in medicinal chemistry · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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

4 authors at 3 institutions in 2 countries.

Jiamei ShenChina-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China; Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.
Radhika RastogiDepartment of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.
Xiaokun GengChina-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China; Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA; Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing, China.
Yuchuan DingDepartment of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.
Wayne State University · USBeijing Luhe Hospital Affiliated to Capital Medical University · CNXiaomi (China) · CN

Funding

Reducing Brain Hyperglycolysis: A Novel Strategy for Hyperglycemia after StrokeI01RX001964 · VA · JOHN D DINGELL VA MEDICAL CENTER · PI DING, YUCHUAN · 2016 to 2020
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RRD VA I01 RX001964
6 · The paper itself

Abstract

Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important cellular functions, including the facilitation of adaptive immunity. In pathogenic circumstances, however, excess reactive oxygen species generated by NOX promotes apoptotic cell death. In ischemic stroke, in particular, it has been shown that both NOX activation and derangements in glucose metabolism result in increased apoptosis. Moreover, recent studies have established that glucose, as a NOX substrate, plays a vital role in the pathogenesis of reperfusion injury. Thus, NOX inhibition has the potential to mitigate the deleterious impact of hyperglycemia on stroke. In this paper, we provide an overview of this research, coupled with a discussion of its implications for the development of NOX inhibition as a strategy for the treatment of ischemic stroke. Both inhibition using apocynin, as well as the prospect of developing more specific inhibitors based on what is now understood of the biology of NOX assembly and activation, will be highlighted in the course of our discussion.

Indexed as

hyperglycolysisischemia/reperfusionNADPHneuroprotectionnicotinamide adenine dinucleotide phosphate oxidasenicotinamide adenine dinucleotide phosphate oxidase inhibitorsNOXreactive oxygen speciesstroke

Identifiers

PMID30761998
PMCPMC6404502
OpenAlexW2914337889

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.