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FGF/FGFR Pathways in Multiple Sclerosis and in Its Disease Models.

Ranjithkumar Rajendran1, Gregor Böttiger1, Christine Stadelmann2

  • 1Experimental Neurology, Department of Neurology, University of Giessen, Klinikstrasse 33, 35385 Giessen, Germany.

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Fibroblast growth factor (FGF) signaling influences inflammation and remyelination in multiple sclerosis (MS). Inhibiting FGF receptors (FGFRs) may reduce inflammation and promote myelin repair in MS.

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AktBDNFEAEERKFGFFGFRLINGO-1SEMA3Amultiple sclerosis

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Area of Science:

  • Neuroimmunology
  • Neurodegenerative diseases
  • Cell signaling

Background:

  • Multiple sclerosis (MS) is a chronic CNS disease characterized by inflammation, demyelination, and neurodegeneration.
  • Oligodendrocyte and myelin damage is central to MS pathology, with impaired remyelination.
  • Fibroblast growth factor (FGF) signaling is implicated in MS, with FGF2 potentially promoting inflammation and FGF1 aiding remyelination.

Purpose of the Study:

  • To review the role of FGF signaling in MS.
  • To explore the therapeutic potential of targeting FGF signaling pathways for MS treatment.

Main Methods:

  • Analysis of post-mortem MS tissue.
  • Investigation of FGF2 and FGF1 roles in MOG35-55-induced experimental autoimmune encephalomyelitis (EAE) in mice.
  • Specific deletion of FGF receptors (FGFRs) in oligodendrocytes in the EAE model.
  • Assessment of inflammatory cell infiltration, myelin and axon integrity, and molecular signaling pathways (ERK/Akt, BDNF).

Main Results:

  • FGF2 expression correlated with inflammation and inversely with myelination in MS.
  • Targeting FGFRs in oligodendrocytes in EAE reduced inflammation and demyelination.
  • FGFR inhibition modulated ERK/Akt phosphorylation, brain-derived neurotrophic factor levels, and remyelination inhibitor expression.

Conclusions:

  • FGF signaling plays a complex role in MS pathogenesis, influencing both inflammation and remyelination.
  • Inhibitors of FGF receptors (FGFRs), currently in cancer trials, represent a potential therapeutic strategy for MS.
  • Targeting FGFRs may reduce CNS inflammation and promote remyelination in MS and EAE models.