Evidence map›Paper›PMID 28208701›Full record

ReviewInternational journal of molecular sciences2017

Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis.

Cecilia Rajda, Dániel Pukoli, Zsuzsanna Bende, Zsófia Majláth, László Vécsei

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Altered Erythrocyte Function via TLR9-ox-mtDNA Binding Links Mitochondrial Oxidative Damage to Systemic Inflammation in Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  4. Article
  5. Role of isoflavones in multiple sclerosis.IBRO neuroscience reports · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Acai Berry (Life (Basel, Switzerland) · 2023
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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 2 institutions in 1 country.

Cecilia RajdaDepartment of Neurology, University of Szeged, 6725 Szeged, Hungary. rajda.cecilia@med.u-szeged.hu.
Dániel PukoliDepartment of Neurology, University of Szeged, 6725 Szeged, Hungary. pukoli.daniel@med.u-szeged.hu.
Zsuzsanna BendeDepartment of Neurology, University of Szeged, 6725 Szeged, Hungary. bendzsu@gmail.com.
Zsófia MajláthDepartment of Neurology, University of Szeged, 6725 Szeged, Hungary. majlathzsofia@gmail.com.
László VécseiDepartment of Neurology, University of Szeged, 6725 Szeged, Hungary. vecsei.laszlo@med.u-szeged.hu.
University of Szeged · HUBM Központi Kórház · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). There is increasing evidence that MS is not only characterized by immune mediated inflammatory reactions, but also by neurodegenerative processes. There is cumulating evidence that neurodegenerative processes, for example mitochondrial dysfunction, oxidative stress, and glutamate (Glu) excitotoxicity, seem to play an important role in the pathogenesis of MS. The alteration of mitochondrial homeostasis leads to the formation of excitotoxins and redox disturbances. Mitochondrial dysfunction (energy disposal failure, apoptosis, etc.), redox disturbances (oxidative stress and enhanced reactive oxygen and nitrogen species production), and excitotoxicity (Glu mediated toxicity) may play an important role in the progression of the disease, causing axonal and neuronal damage. This review focuses on the mechanisms of mitochondrial dysfunction (including mitochondrial DNA (mtDNA) defects and mitochondrial structural/functional changes), oxidative stress (including reactive oxygen and nitric species), and excitotoxicity that are involved in MS and also discusses the potential targets and tools for therapeutic approaches in the future.

Indexed as

Oxidation-ReductionAnimalsBiomarkersBlood-Brain BarrierDisease Models, AnimalDisease ProgressionGlutamic AcidHumansMitochondriaMultiple SclerosisNeurotoxinsOxidative StressReceptors, GlutamateBiomarkersGlutamic AcidNeurotoxinsReceptors, Glutamatebiomarkerexcitotoxinglutamatemitochondriamultiple sclerosisneurodegenerationoxidative stress

Identifiers

PMID28208701
PMCPMC5343888
OpenAlexW2587637294

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.