Evidence map›Paper›PMID 21947442›Full record

ReviewCellular and molecular life sciences : CMLS2012

Reactive oxygen species and the neuronal fate.

Karen A M Kennedy, Shelley D E Sandiford, Ilona S Skerjanc, Shawn S-C Li

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
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  7. NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024
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  17. Oxidative Stress as a Common Key Event in Developmental Neurotoxicity.Oxidative medicine and cellular longevity · 2021
    Review
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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

4 authors at 2 institutions in 1 country.

Karen A M KennedyDepartment of Biochemistry, Medical Sciences Building, The University of Western Ontario, London, ON, Canada.
Shelley D E Sandiford
Ilona S Skerjanc
Shawn S-C Li
Western University · CAUniversity of Ottawa · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Aberrant or elevated levels of reactive oxygen species (ROS) can mediate deleterious cellular effects, including neuronal toxicity and degeneration observed in the etiology of a number of pathological conditions, including Alzheimer's and Parkinson's diseases. Nevertheless, ROS can be generated in a controlled manner and can regulate redox sensitive transcription factors such as NFκB, AP-1 and NFAT. Moreover, ROS can modulate the redox state of tyrosine phosphorylated proteins, thereby having an impact on many transcriptional networks and signaling cascades important for neurogenesis. A large body of literature links the controlled generation of ROS at low-to-moderate levels with the stimulation of differentiation in certain developmental programs such as neurogenesis. In this regard, ROS are involved in governing the acquisition of the neural fate-from neural induction to the elaboration of axons. Here, we summarize and discuss the growing body of literature that describe a role for ROS signaling in neuronal development.

Indexed as

NeurogenesisAnimalsFemaleHumansMaleMiceNADPH OxidasesNervous SystemNeuronsReactive Oxygen SpeciesSignal TransductionNADPH OxidasesReactive Oxygen Species

Identifiers

PMID21947442
PMCPMC11114775
OpenAlexW2021375247

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.