Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis.
PKR
SARS-CoV2
TAU
beta catenin
degenerative disease
inflammation
interferon
small-molecule inhibitors
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
21 11 2021
21 11 2021
Historique:
received:
01
10
2021
revised:
18
11
2021
accepted:
19
11
2021
entrez:
27
11
2021
pubmed:
28
11
2021
medline:
15
12
2021
Statut:
epublish
Résumé
Idiopathic or sporadic inclusion body myositis (IBM) is the leading age-related (onset >50 years of age) autoimmune muscular pathology, resulting in significant debilitation in affected individuals. Once viewed as primarily a degenerative disorder, it is now evident that much like several other neuro-muscular degenerative disorders, IBM has a major autoinflammatory component resulting in chronic inflammation-induced muscle destruction. Thus, IBM is now considered primarily an inflammatory pathology. To date, there is no effective treatment for sporadic inclusion body myositis, and little is understood about the pathology at the molecular level, which would offer the best hopes of at least slowing down the degenerative process. Among the previously examined potential molecular players in IBM is glycogen synthase kinase (GSK)-3, whose role in promoting TAU phosphorylation and inclusion bodies in Alzheimer's disease is well known. This review looks to re-examine the role of GSK3 in IBM, not strictly as a promoter of TAU and Abeta inclusions, but as a novel player in the innate immune system, discussing some of the recent roles discovered for this well-studied kinase in inflammatory-mediated pathology.
Identifiants
pubmed: 34831477
pii: cells10113255
doi: 10.3390/cells10113255
pmc: PMC8625526
pii:
doi:
Substances chimiques
Glycogen Synthase Kinase 3
EC 2.7.11.26
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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