Evidence map›Paper›PMID 38247808›Full record

ReviewCells2024

Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.

Zhixin Lei, Wensheng Lin

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

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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.

Zhixin LeiSchool of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, Wuhan 430070, China.
Wensheng LinDepartment of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.ORCID 0000-0003-4931-7642

Funding

Mechanisms for maintaining ER protein homeostasis in myelinating cellsR01NS105689 · NINDS · UNIVERSITY OF MINNESOTA · PI LIN, WENSHENG · 2018 to 2022
$1.7M
NIH HHS NS105689NINDS NIH HHS R01 NS105689
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic autoimmune inflammatory demyelinating disease of the central nervous system (CNS), which is triggered by an autoimmune assault targeting oligodendrocytes and myelin. Recent research indicates that the demise of oligodendrocytes due to an autoimmune attack contributes significantly to the pathogenesis of MS and its animal model experimental autoimmune encephalomyelitis (EAE). A key challenge in MS research lies in comprehending the mechanisms governing oligodendrocyte viability and devising therapeutic approaches to enhance oligodendrocyte survival. Here, we provide an overview of recent findings that highlight the contributions of oligodendrocyte death to the development of MS and EAE and summarize the current literature on the mechanisms governing oligodendrocyte viability in these diseases.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsCentral Nervous SystemMyelin SheathOligodendrogliaexperimental autoimmune encephalomyelitisIFN-γmitochondriamultiple sclerosismyelinNF-κBoligodendrocyteoxidative stressunfolded protein response

Identifiers

PMID38247808
PMCPMC10814231

What OpenQuestion holds

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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.