Evidence map›Paper›PMID 24148000›Full record

ReviewBritish journal of pharmacology2014

Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target?

H Muyderman, T Chen

Abstract 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 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

67 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  8. Rab14 promotes Parkin-mediated mitophagy.Molecular biology of the cell · 2025
    Article
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  10. Article
  11. Article
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  15. Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024
    Article
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  17. Review
  18. Review
  19. Review
  20. Review

7 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.

H MuydermanCentre for Neuroscience, Discipline of Medical Biochemistry, Flinders Medical Science and Technology, School of Medicine, Flinders University, Adelaide, SA, Australia.
T Chen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by the selective death of upper and lower motor neurons which ultimately leads to paralysis and ultimately death. Pathological changes in ALS are closely associated with pronounced and progressive changes in mitochondrial morphology, bioenergetics and calcium homeostasis. Converging evidence suggests that impaired mitochondrial function could be pivotal in the rapid neurodegeneration of this condition. In this review, we provide an update of recent advances in understanding mitochondrial biology in the pathogenesis of ALS and highlight the therapeutic value of pharmacologically targeting mitochondrial biology to slow disease progression.

Indexed as

Amyotrophic Lateral SclerosisAnimalsCalciumCell DeathEnergy MetabolismGlutathioneHomeostasisHumansMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMolecular Targeted TherapyMutationOxidative StressSuperoxide DismutaseSuperoxide Dismutase-1CalciumGlutathioneMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreSOD1 protein, humanSuperoxide DismutaseSuperoxide Dismutase-1amyotrophic lateral sclerosiscell deathmitochondriaSOD-1TDP-43therapeutic

Identifiers

PMID24148000
PMCPMC3976630

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.