Aging, Cellular Senescence, and Progressive Multiple Sclerosis.
cellular senescence
inflammation
multiple sclerosis
neurodegeneration
neuroprotection
remyelination
senolytics
Journal
Frontiers in cellular neuroscience
ISSN: 1662-5102
Titre abrégé: Front Cell Neurosci
Pays: Switzerland
ID NLM: 101477935
Informations de publication
Date de publication:
2020
2020
Historique:
received:
30
03
2020
accepted:
22
05
2020
entrez:
23
7
2020
pubmed:
23
7
2020
medline:
23
7
2020
Statut:
epublish
Résumé
Aging is one of the most important risk factors for the development of several neurodegenerative diseases including progressive multiple sclerosis (MS). Cellular senescence (CS) is a key biological process underlying aging. Several stressors associated with aging and MS pathology, such as oxidative stress, mitochondrial dysfunction, cytokines and replicative exhaustion are known triggers of cellular senescence. Senescent cells exhibit stereotypical metabolic and functional changes, which include cell-cycle arrest and acquiring a pro-inflammatory phenotype secreting cytokines, growth factors, metalloproteinases and reactive oxygen species. They accumulate with aging and can convert neighboring cells to senescence in a paracrine manner. In MS, accelerated cellular senescence may drive disease progression by promoting chronic non-remitting inflammation, loss or altered immune, glial and neuronal function, failure of remyelination, impaired blood-brain barrier integrity and ultimately neurodegeneration. Here we discuss the evidence linking cellular senescence to the pathogenesis of MS and the putative role of senolytic and senomorphic agents as neuroprotective therapies in tackling disease progression.
Identifiants
pubmed: 32694983
doi: 10.3389/fncel.2020.00178
pmc: PMC7338849
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
178Informations de copyright
Copyright © 2020 Papadopoulos, Magliozzi, Mitsikostas, Gorgoulis and Nicholas.
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