Mostrar el registro sencillo del ítem

dc.contributor.authorVaras R.
dc.contributor.authorOrtiz F.C.
dc.date.accessioned2020-09-02T22:29:55Z
dc.date.available2020-09-02T22:29:55Z
dc.date.issued2019
dc.identifier10.2174/1381612825666191216125725
dc.identifier.citation25, 45, 4755-4762
dc.identifier.issn13816128
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6517
dc.descriptionMyelin is a specialized membrane allowing for saltatory conduction of action potentials in neurons, an essential process to achieve the normal communication across the nervous system. Accordingly, in diseases characterized by the loss of myelin and myelin forming cells-oligodendrocytes in the CNS-, patients show severe neurological disabilities. After a demyelinated insult, microglia, astrocytes and oligodendrocyte precursor cells invade the lesioned area initiating a spontaneous process of myelin repair (i.e. remyelination). A preserved hallmark of this neuroinflammatory scenario is a local increase of oxidative stress, where several cytokines and chemokines are released by glial and other cells. This generates an environment that determines cell interaction resulting in oligodendrocyte maturity and the ability to synthesize new myelin. Herein we review the main features of the regulatory aspect of these molecules based on recent findings and propose new putative signal molecules involved in the remyelination process, focused in the etiology of Multiple Sclerosis, one of the main demyelinating diseases causing disabilities in the population. © 2019 Bentham Science Publishers.
dc.language.isoen
dc.publisherBentham Science Publishers
dc.subjectGlial cross-talk
dc.subjectMicroglia
dc.subjectMultiple Sclerosis
dc.subjectNeuroinflammation
dc.subjectOxidative stress
dc.subjectRemyelination
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinterleukin 17
dc.subjectinterleukin 1beta
dc.subjectinterleukin 22
dc.subjectinterleukin 23
dc.subjectinterleukin 4
dc.subjectinterleukin 6
dc.subjectmonocyte chemotactic protein 1
dc.subjectmuscarinic receptor blocking agent
dc.subjectocrelizumab
dc.subjectreactive oxygen metabolite
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase 2
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase 4
dc.subjecttoll like receptor 4
dc.subjecttranscription factor Nrf2
dc.subjecttransforming growth factor beta
dc.subjecttumor necrosis factor
dc.subjectCD4+ T lymphocyte
dc.subjectdemyelinating disease
dc.subjectdisease severity
dc.subjectdrug targeting
dc.subjectenzyme activity
dc.subjectgene expression
dc.subjectglia cell
dc.subjecthuman
dc.subjectmultiple sclerosis
dc.subjectnervous system inflammation
dc.subjectnonhuman
dc.subjectoligodendrocyte precursor cell
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectremyelinization
dc.subjectReview
dc.subjectTh17 cell
dc.subjectcell communication
dc.subjectcytology
dc.subjectdemyelinating disease
dc.subjectglia
dc.subjectinflammation
dc.subjectmultiple sclerosis
dc.subjectmyelin sheath
dc.subjectoligodendroglia
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectCell Communication
dc.subjectDemyelinating Diseases
dc.subjectHumans
dc.subjectInflammation
dc.subjectMultiple Sclerosis
dc.subjectMyelin Sheath
dc.subjectNeuroglia
dc.subjectOligodendroglia
dc.subjectOxidative Stress
dc.titleNeuroinflammation in demyelinating diseases: Oxidative stress as a modulator of glial cross-talk
dc.typeReview


Ficheros en el ítem

Thumbnail

Este ítem aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo del ítem