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Mediators of oligodendrocyte differentiation during remyelination

期刊

FEBS LETTERS
卷 585, 期 23, 页码 3730-3737

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2011.04.037

关键词

Cytokines; Chemokines; Growth factor; MicroRNA; Multiple sclerosis; Transcription factor

资金

  1. National Institutes of Health (NIH)/National Institute of Neurological Disorders and Stroke [NS059560]
  2. National Multiple Sclerosis Society

向作者/读者索取更多资源

Myelin, a dielectric sheath that wraps large axons in the central and peripheral nervous systems, is essential for proper conductance of axon potentials. In multiple sclerosis (MS), autoimmune-mediated damage to myelin within the central nervous system (CNS) leads to progressive disability primarily due to limited endogenous repair of demyelination with associated axonal pathology. While treatments are available to limit demyelination, no treatments are available to promote myelin repair. Studies examining the molecular mechanisms that promote remyelination are therefore essential for identifying therapeutic targets to promote myelin repair and thereby limit disability in MS. Here, we present our current understanding of the critical extracellular and intracellular pathways that regulate the remyelinating capabilities of oligodendrocyte precursor cells (OPCs) within the adult CNS. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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