Evidence map›Paper›PMID 37629092›Full record

ReviewInternational journal of molecular sciences2023

Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis.

Eneritz López-Muguruza, Carlos Matute

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
17.7field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 101 citations in OpenAlex.

  1. Honokiol attenuates neuroinflammation and enhances remyelination in mouse models of multiple sclerosis through PPARγ-mediated ERK/AKT signalling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  8. White matter injury after brain ischemia.Experimental neurology · 2026
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8 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 at 1 institution in 1 country.

Eneritz López-MuguruzaAchucarro Basque Center for Neuroscience, 48940 Leioa, Spain.
Carlos MatuteAchucarro Basque Center for Neuroscience, 48940 Leioa, Spain.ORCID 0000-0001-8672-711X
University of the Basque Country · ES

Funding

Biomedical Research Networking Center on Neurodegenerative Diseases CB06/05/0076
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a complex autoimmune disease of the central nervous system (CNS), characterized by demyelination and neurodegeneration. Oligodendrocytes play a vital role in maintaining the integrity of myelin, the protective sheath around nerve fibres essential for efficient signal transmission. However, in MS, oligodendrocytes become dysfunctional, leading to myelin damage and axonal degeneration. Emerging evidence suggests that metabolic changes, including mitochondrial dysfunction and alterations in glucose and lipid metabolism, contribute significantly to the pathogenesis of MS. Mitochondrial dysfunction is observed in both immune cells and oligodendrocytes within the CNS of MS patients. Impaired mitochondrial function leads to energy deficits, affecting crucial processes such as impulse transmission and axonal transport, ultimately contributing to neurodegeneration. Moreover, mitochondrial dysfunction is linked to the generation of reactive oxygen species (ROS), exacerbating myelin damage and inflammation. Altered glucose metabolism affects the energy supply required for oligodendrocyte function and myelin synthesis. Dysregulated lipid metabolism results in changes to the composition of myelin, affecting its stability and integrity. Importantly, low levels of polyunsaturated fatty acids in MS are associated with upregulated lipid metabolism and enhanced glucose catabolism. Understanding the intricate relationship between these mechanisms is crucial for developing targeted therapies to preserve myelin and promote neurological recovery in individuals with MS. Addressing these metabolic aspects may offer new insights into potential therapeutic strategies to halt disease progression and improve the quality of life for MS patients.

Indexed as

Multiple SclerosisMyelin SheathEnergy MetabolismGlucoseHumansOligodendrogliaQuality of LifeGlucoseaxonal damagedemyelinationdysmyelinationlipidsmitochondrianeurodegenerationprogressive multiple sclerosisremyelinationrepair

Identifiers

PMID37629092
PMCPMC10454078
OpenAlexW4385978702

What Socratic 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 Socratic graph.