Evidence map›Paper›PMID 23727323›Full record

ReviewFree radical biology & medicine2013

SOD2 in mitochondrial dysfunction and neurodegeneration.

James M Flynn, Simon Melov

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed
7.6field-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

216 citing papers in PubMed, 369 citations in OpenAlex.

  1. Article
  2. Review
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  8. bioRxiv : the preprint server for biology · 2026
    Article
  9. Polyunsaturated fatty acid metabolism in the retinal pigment epithelium and its association with outer retinal disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  10. Article
  11. bioRxiv : the preprint server for biology · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
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  17. Review
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  20. Article

156 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

2 authors at 1 institution in 1 country.

James M FlynnBuck Institute for Research on Aging, Novato, CA 94945, USA.
Simon MelovBuck Institute for Research on Aging, Novato, CA 94945, USA. Electronic address: SMelov@buckinstitute.org.
Buck Institute for Research on Aging · US

Funding

Training in Basic Research on Aging and Age-Related DiseaseT32AG000266 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Lisa M Ellerby · 1998 to 2026
$13.8M
PROTEOMICSP01AG025901 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GIBSON, BRADFORD WAYNE · 2007 to 2011
$8.6M
Core--RESEARCH DEVELOPMENTP30AG025708 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2005 to 2009
$3.7M
Procedures for Testing Older Driving CapabilitiesR44AG018675 · NIA · SYSTEMS TECHNOLOGY, INC. · PI ALLEN, R. WADE · 2003 to 2004
$744k
Procedures for Testing Older Driving CapabilitiesR43AG018675 · NIA · SYSTEMS TECHNOLOGY, INC. · PI ALLEN, R. WADE · 2001 to 2001
$106k
NIA NIH HHS AG18675NIA NIH HHS P01 AG025901NIA NIH HHS P01AG025901NIA NIH HHS P30 AG025708NIA NIH HHS P30AG025708NIA NIH HHS R44 AG018675NIA NIH HHS T32 AG000266NIA NIH HHS T32AG000266
6 · The paper itself

Abstract

The brain is a highly metabolically active tissue that critically relies on oxidative phosphorylation as a means for maintaining energy. One result of this process is the production of potentially damaging radicals such as the superoxide anion (O2(-)). Superoxide has the capacity to damage components of the electron transport chain and other cellular constituents. Eukaryotic systems have evolved defenses against such damaging moieties, the chief member of which is superoxide dismutase (SOD2), an enzyme that efficiently converts superoxide to the less reactive hydrogen peroxide (H2O2), which can freely diffuse across the mitochondrial membrane. Loss of SOD2 activity can result in numerous pathological phenotypes in metabolically active tissues, particularly within the central nervous system. We review SOD2's potential involvement in the progression of neurodegenerative diseases such as stroke and Alzheimer and Parkinson diseases, as well as its potential role in "normal" age-related cognitive decline. We also examine in vivo models of endogenous oxidative damage based upon the loss of SOD2 and associated neurological phenotypes in relation to human neurodegenerative disorders.

Indexed as

Oxidation-ReductionBrainHumansHydrogen PeroxideMitochondriaMitochondrial DiseasesNeurodegenerative DiseasesOxidative PhosphorylationSuperoxide DismutaseSuperoxide Dismutase 2SuperoxidesHydrogen PeroxideSuperoxide DismutaseSuperoxide Dismutase 2SuperoxidesAgingFree radicalsMitochondriaNeurodegenerationOxidative stressSuperoxide dismutase

Identifiers

PMID23727323
PMCPMC3811078
OpenAlexW2058906042

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.