Evidence map›Paper›PMID 23533690›Full record

ReviewOxidative medicine and cellular longevity2013

Redox regulation in amyotrophic lateral sclerosis.

Sonam Parakh, Damian M Spencer, Mark A Halloran, Kai Y Soo, Julie D Atkin

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 80 citations in OpenAlex.

  1. Plasma exchange with albumin replacement and disease progression in amyotrophic lateral sclerosis: a pilot study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Trial
  2. Review
  3. Article
  4. Review
  5. Update on the pathological roles of prostaglandin ETranslational neurodegeneration · 2023
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Dysregulation of IGF-1/GLP-1 signaling in the progression of ALS: potential target activators and influences on neurological dysfunctions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  13. Progressive Mitochondrial SOD1International journal of molecular sciences · 2021
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Sonam ParakhDepartment of Biochemistry, La Trobe Institute for Molecular Science, La Trobe University, Vic 3086, Australia.
Damian M Spencer
Mark A Halloran
Kai Y Soo
Julie D Atkin
La Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that results from the death of upper and lower motor neurons. Due to a lack of effective treatment, it is imperative to understand the underlying mechanisms and processes involved in disease progression. Regulations in cellular reduction/oxidation (redox) processes are being increasingly implicated in disease. Here we discuss the possible involvement of redox dysregulation in the pathophysiology of ALS, either as a cause of cellular abnormalities or a consequence. We focus on its possible role in oxidative stress, protein misfolding, glutamate excitotoxicity, lipid peroxidation and cholesterol esterification, mitochondrial dysfunction, impaired axonal transport and neurofilament aggregation, autophagic stress, and endoplasmic reticulum (ER) stress. We also speculate that an ER chaperone protein disulphide isomerase (PDI) could play a key role in this dysregulation. PDI is essential for normal protein folding by oxidation and reduction of disulphide bonds, and hence any disruption to this process may have consequences for motor neurons. Addressing the mechanism underlying redox regulation and dysregulation may therefore help to unravel the molecular mechanism involved in ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAutophagyAxonal TransportCholesterolEndoplasmic Reticulum StressGlutamic AcidHumansLipid PeroxidationMitochondriaOxidation-ReductionOxidative StressProtein Disulfide-IsomerasesCholesterolGlutamic AcidProtein Disulfide-Isomerases

Identifiers

PMID23533690
PMCPMC3596916
OpenAlexW1995562965

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.