Evidence map›Paper›PMID 23422879›Full record

ReviewNeurochemistry international2013

Oxidative stress, DNA damage, and the telomeric complex as therapeutic targets in acute neurodegeneration.

Joshua A Smith, Sookyoung Park, James S Krause, Naren L Banik

Open access · greenAbstract readReview
In one paragraph

Review in Neurochemistry international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.2field-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

70 citing papers in PubMed, 166 citations in OpenAlex.

  1. Article
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  4. Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  6. Review
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  15. Review
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  18. The Therapeutic Effect ofMolecules (Basel, Switzerland) · 2022
    Article
  19. Article
  20. Article

10 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

4 authors at 1 institution in 1 country.

Joshua A SmithDivision of Neurology, Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas St., Clinical Sciences Building Room 309, Charleston, SC 29425, USA. smijo@musc.edu
Sookyoung Park
James S Krause
Naren L Banik
Medical University of South Carolina · US

Funding

ROLE OF PROTEINASE IN SPINAL CORD INJURYR01NS031622 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 1994 to 2011
$3.4M
Inflammation and Degeneration of Optic Nerve in EAER01NS065456 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2009 to 2013
$1.6M
Extra-nigral Neurodegeneration in Experimental Parkinson's DiseaseR01NS062327 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2009 to 2013
$1.6M
Hormonal Intervention Protects Axon-myelin to Promote Functional Recovery in SCII01BX001262 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI BANIK, NAREN L · 2013 to 2025
–
BLRD VA I01 BX001262NINDS NIH HHS NS-31622NINDS NIH HHS NS-62327NINDS NIH HHS R01 NS031622NINDS NIH HHS R01 NS062327NINDS NIH HHS R01 NS065456
6 · The paper itself

Abstract

Oxidative stress has been identified as an important contributor to neurodegeneration associated with acute CNS injuries and diseases such as spinal cord injury (SCI), traumatic brain injury (TBI), and ischemic stroke. In this review, we briefly detail the damaging effects of oxidative stress (lipid peroxidation, protein oxidation, etc.) with a particular emphasis on DNA damage. Evidence for DNA damage in acute CNS injuries is presented along with its downstream effects on neuronal viability. In particular, unchecked oxidative DNA damage initiates a series of signaling events (e.g. activation of p53 and PARP-1, cell cycle re-activation) which have been shown to promote neuronal loss following CNS injury. These findings suggest that preventing DNA damage might be an effective way to promote neuronal survival and enhance neurological recovery in these conditions. Finally, we identify the telomere and telomere-associated proteins (e.g. telomerase) as novel therapeutic targets in the treatment of neurodegeneration due to their ability to modulate the neuronal response to both oxidative stress and DNA damage.

Indexed as

DNA DamageOxidative StressTelomereAnimalsHumansMiceMice, TransgenicNeurodegenerative Diseases

Identifiers

PMID23422879
PMCPMC3619128
OpenAlexW2014034103

What OpenQuestion holds

Textmetadata
LicenceTDM
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.