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 language | English (US) |
---|---|
Article number | 116 |
Journal | Cells |
Volume | 13 |
Issue number | 2 |
DOIs | |
State | Published - 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