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Possible Regenerative Effects of Fingolimod (Fty720) in Multiple Sclerosis Disease: An Overview on Remyelination Process Publisher Pubmed



Yazdi A1 ; Ghasemikasman M2, 3 ; Javan M4, 5
Authors
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Authors Affiliations
  1. 1. Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
  3. 3. Neuroscience Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
  4. 4. Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  5. 5. Department of Brain and Cognitive Sciences, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran

Source: Journal of Neuroscience Research Published:2020


Abstract

Fingolimod (FTY720) is a sphingosine 1-phosphate (S1P) receptor analog, which has been approved as an oral immunomodulator for treating relapsing–remitting multiple sclerosis. This drug prevents lymphocyte egression from lymph nodes and reduces the infiltration of inflammatory mediators into the central nervous system. Based on its lipophilic nature, FTY720 passes through the blood–brain barrier and can directly affect neural cells. A notably different subtype of S1P receptors expresses in neural cells, which suggests FTY720 is a drug capable of affecting neural cells. Oligodendrocytes (OLs) are considered as the primary target cells in MS. Remyelination is a process including the proliferation of neural progenitors and oligodendrocyte precursor cells, their migration to the lesion site and their differentiation to mature oligodendrocytes. Experimental and clinical studies have described the impact of FTY720 on endogenous remyelination elements. In this review, we will explain the current clinical and experimental evidence that exists on the effects of FTY720 on remyelination and the underlying mechanisms. © 2019 Wiley Periodicals, Inc.
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