Evidence map›Paper›PMID 24206195›Full record

ReviewBritish journal of pharmacology2014

Mitochondrial metals as a potential therapeutic target in neurodegeneration.

A Grubman, A R White, J R Liddell

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Copper homeostasis and the ubiquitin proteasome system.Metallomics : integrated biometal science · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. The Copper bis(thiosemicarbazone) Complex CuNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Article
  11. Article
  12. Article
  13. Mitochondrial pharmacology: energy, injury and beyond.British journal of pharmacology · 2014
    Article
  14. Review
  15. Review
  16. 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

3 authors at 1 institution in 1 country.

A GrubmanDepartment of Pathology, University of Melbourne, Melbourne, Vic., Australia.
A R White
J R Liddell
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transition metals are critical for enzyme function and protein folding, but in excess can mediate neurotoxic oxidative processes. As mitochondria are particularly vulnerable to oxidative damage due to radicals generated during ATP production, mitochondrial biometal homeostasis must therefore be tightly controlled to safely harness the redox potential of metal enzyme cofactors. Dysregulation of metal functions is evident in numerous neurological disorders including Alzheimer's disease, stroke, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis and Friedrich's ataxia. This review describes the mitochondrial metal defects in these disorders and highlights novel metal-based therapeutic approaches that target mitochondrial metal homeostasis in neurological disorders.

Indexed as

CationsChelating AgentsHomeostasisHumansMitochondriaMolecular Targeted TherapyNeurodegenerative DiseasesTransition ElementsCationsChelating AgentsTransition Elementsbiometal homeostasisCu(atsm)curcumindeferipronemitochondriaMn porphyrinsneurodegenerationstroke

Identifiers

PMID24206195
PMCPMC3976628
OpenAlexW1545394062

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.