Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models

Zhixin Lei, Wensheng Lin

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations

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.

Original languageEnglish (US)
Article number116
JournalCells
Volume13
Issue number2
DOIs
StatePublished - Jan 2024

Bibliographical note

Publisher Copyright:
© 2024 by the authors.

Keywords

  • IFN-γ
  • NF-κB
  • experimental autoimmune encephalomyelitis
  • mitochondria
  • multiple sclerosis
  • myelin
  • oligodendrocyte
  • oxidative stress
  • unfolded protein response

PubMed: MeSH publication types

  • Journal Article
  • Review
  • Research Support, Non-U.S. Gov't

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