Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis

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 n...

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Autores principales:	Manuela Piazzi, Alberto Bavelloni, Vittoria Cenni, Irene Faenza, William L. Blalock
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	inflammation degenerative disease PKR beta catenin interferon SARS-CoV2 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/50b65513378841e1aa7a4d66684e76ad
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spelling	oai:doaj.org-article:50b65513378841e1aa7a4d66684e76ad2021-11-25T17:13:20ZRevisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis10.3390/cells101132552073-4409https://doaj.org/article/50b65513378841e1aa7a4d66684e76ad2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3255https://doaj.org/toc/2073-4409Idiopathic 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.Manuela PiazziAlberto BavelloniVittoria CenniIrene FaenzaWilliam L. BlalockMDPI AGarticleinflammationdegenerative diseasePKRbeta catenininterferonSARS-CoV2Biology (General)QH301-705.5ENCells, Vol 10, Iss 3255, p 3255 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	inflammation degenerative disease PKR beta catenin interferon SARS-CoV2 Biology (General) QH301-705.5
spellingShingle	inflammation degenerative disease PKR beta catenin interferon SARS-CoV2 Biology (General) QH301-705.5 Manuela Piazzi Alberto Bavelloni Vittoria Cenni Irene Faenza William L. Blalock Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis
description	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.
format	article
author	Manuela Piazzi Alberto Bavelloni Vittoria Cenni Irene Faenza William L. Blalock
author_facet	Manuela Piazzi Alberto Bavelloni Vittoria Cenni Irene Faenza William L. Blalock
author_sort	Manuela Piazzi
title	Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis
title_short	Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis
title_full	Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis
title_fullStr	Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis
title_full_unstemmed	Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis
title_sort	revisiting the role of gsk3, a modulator of innate immunity, in idiopathic inclusion body myositis
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/50b65513378841e1aa7a4d66684e76ad
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Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis

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