Signaling mechanisms involved in the regulation of remyelination in multiple sclerosis: a mini review

J Mol Med (Berl). 2023 Jun;101(6):637-644. doi: 10.1007/s00109-023-02312-9. Epub 2023 Apr 21.

Abstract

Multiple sclerosis is an autoimmune neurodegenerative disease of the CNS that causes progressive disabilities, owing to CNS axon degeneration as a late result of demyelination. In the search for the prevention of axonal loss, mitigating inflammatory attacks in the CNS and myelin restoration are two possible approaches. As a result, therapies that target diverse signaling pathways involved in neuroprotection and remyelination have the potential to overcome the challenges in the development of multiple sclerosis treatments. LINGO1 (Leucine rich repeat and Immunoglobulin domain containing, Nogo receptor- interaction protein), AKT/PIP3/mTOR, Notch, Wnt, RXR (Retinoid X receptor gamma), and Nrf2 (nuclear factor erythroid 2-related factor 2) signaling pathways are highlighted in this section. This article reviews the present knowledge regarding numerous signaling pathways and their functions in regulating remyelination in multiple sclerosis pathogenesis. These pathways are potential biomarkers and therapeutic targets in MS.

Keywords: AKT/mTOR; LINGO1; Multiple sclerosis; Notch; Nrf2; RXR-γ; Remyelination; Wnt/β Catenin.

Publication types

  • Review

MeSH terms

  • Humans
  • Multiple Sclerosis* / drug therapy
  • Myelin Sheath / metabolism
  • Myelin Sheath / pathology
  • Neurodegenerative Diseases* / metabolism
  • Oligodendroglia / metabolism
  • Oligodendroglia / pathology
  • Remyelination*