• Treffer 3 von 8
Zurück zur Trefferliste

FGF/FGFR pathways in multiple sclerosis and in its disease models

Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-236594
  • Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS) affecting more than two million people worldwide. In MS, oligodendrocytes and myelin sheaths are destroyed by autoimmune-mediated inflammation, while remyelination is impaired. Recent investigations of post-mortem tissue suggest that Fibroblast growth factor (FGF) signaling may regulate inflammation and myelination in MS. FGF2 expression seems to correlate positively with macrophages/microglia and negatively with myelination; FGF1Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS) affecting more than two million people worldwide. In MS, oligodendrocytes and myelin sheaths are destroyed by autoimmune-mediated inflammation, while remyelination is impaired. Recent investigations of post-mortem tissue suggest that Fibroblast growth factor (FGF) signaling may regulate inflammation and myelination in MS. FGF2 expression seems to correlate positively with macrophages/microglia and negatively with myelination; FGF1 was suggested to promote remyelination. In myelin oligodendrocyte glycoprotein (MOG)\(_{35–55}\)-induced experimental autoimmune encephalomyelitis (EAE), systemic deletion of FGF2 suggested that FGF2 may promote remyelination. Specific deletion of FGF receptors (FGFRs) in oligodendrocytes in this EAE model resulted in a decrease of lymphocyte and macrophage/microglia infiltration as well as myelin and axon degeneration. These effects were mediated by ERK/Akt phosphorylation, a brain-derived neurotrophic factor, and downregulation of inhibitors of remyelination. In the first part of this review, the most important pharmacotherapeutic principles for MS will be illustrated, and then we will review recent advances made on FGF signaling in MS. Thus, we will suggest application of FGFR inhibitors, which are currently used in Phase II and III cancer trials, as a therapeutic option to reduce inflammation and induce remyelination in EAE and eventually MS.zeige mehrzeige weniger

Volltext Dateien herunterladen

Metadaten exportieren

Weitere Dienste

Teilen auf Twitter Suche bei Google Scholar Statistik - Anzahl der Zugriffe auf das Dokument
Metadaten
Autor(en): Ranjithkumar Rajendran, Gregor Böttiger, Christine Stadelmann, Srikanth Karnati, Martin Berghoff
URN:urn:nbn:de:bvb:20-opus-236594
Dokumentart:Artikel / Aufsatz in einer Zeitschrift
Institute der Universität:Medizinische Fakultät / Institut für Anatomie und Zellbiologie
Sprache der Veröffentlichung:Englisch
Titel des übergeordneten Werkes / der Zeitschrift (Englisch):Cells
ISSN:2073-4409
Erscheinungsjahr:2021
Band / Jahrgang:10
Heft / Ausgabe:4
Aufsatznummer:884
Originalveröffentlichung / Quelle:Cells (2021) 10:4, 884. https://doi.org/10.3390/cells10040884
DOI:https://doi.org/10.3390/cells10040884
Allgemeine fachliche Zuordnung (DDC-Klassifikation):6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Freie Schlagwort(e):Akt; BDNF; EAE; ERK; FGF; FGFR; LINGO-1; SEMA3A; multiple sclerosis
Datum der Freischaltung:10.08.2022
Datum der Erstveröffentlichung:13.04.2021
Lizenz (Deutsch):License LogoCC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International