Evidence map›Paper›PMID 32144830›Full record

ReviewAngewandte Chemie (International ed. in English)2021

Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.

Benjamin G Trist, James B Hilton, Dominic J Hare, Peter J Crouch, Kay L Double

Open access · hybridAbstract readReview
In one paragraph

Review in Angewandte Chemie (International ed. in English), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
7.5field-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

125 citing papers in PubMed, 207 citations in OpenAlex.

  1. Article
  2. Review
  3. SOD1 Overexpression Alleviates HAntioxidants (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Molecular Modulation of the Crosstalk Between TDP-43 and SOD1.International journal of molecular sciences · 2026
    Article
  12. Nose-to-brain delivery of a SOD1-stabilizing small molecule ameliorates pathology in an ALS mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Enzyme Immobilization in Porous Crystals via Cage Encapsulation.Angewandte Chemie (International ed. in English) · 2025
    Article
  20. Article

65 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

5 authors at 3 institutions in 1 country.

Benjamin G TristBrain and Mind Centre and Discipline of Pharmacology, The University of Sydney, Camperdown, Sydney, New South Wales, 2050, Australia.ORCID 0000-0002-0712-399X
James B HiltonDepartment of Pharmacology and Therapeutics, The University of Melbourne, Parkville, Victoria, 3052, Australia.
Dominic J HareBrain and Mind Centre and Discipline of Pharmacology, The University of Sydney, Camperdown, Sydney, New South Wales, 2050, Australia.
Peter J CrouchDepartment of Pharmacology and Therapeutics, The University of Melbourne, Parkville, Victoria, 3052, Australia.
Kay L DoubleBrain and Mind Centre and Discipline of Pharmacology, The University of Sydney, Camperdown, Sydney, New South Wales, 2050, Australia.
The University of Melbourne · AUThe University of Sydney · AUUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cu/Zn superoxide dismutase (SOD1) is a frontline antioxidant enzyme catalysing superoxide breakdown and is important for most forms of eukaryotic life. The evolution of aerobic respiration by mitochondria increased cellular production of superoxide, resulting in an increased reliance upon SOD1. Consistent with the importance of SOD1 for cellular health, many human diseases of the central nervous system involve perturbations in SOD1 biology. But far from providing a simple demonstration of how disease arises from SOD1 loss-of-function, attempts to elucidate pathways by which atypical SOD1 biology leads to neurodegeneration have revealed unexpectedly complex molecular characteristics delineating healthy, functional SOD1 protein from that which likely contributes to central nervous system disease. This review summarises current understanding of SOD1 biology from SOD1 genetics through to protein function and stability.

Indexed as

AntioxidantsBiocatalysisCentral Nervous System DiseasesEnzyme StabilityHumansSuperoxide Dismutase-1SuperoxidesAntioxidantsSOD1 protein, humanSuperoxide Dismutase-1SuperoxidesantioxidantscopperCu/Zn superoxide dismutaseneurodegenerationprotein misfolding

Identifiers

PMID32144830
PMCPMC8247289
OpenAlexW3009127249

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.