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

Manuela Piazzi, Alberto Bavelloni, Vittoria Cenni, Irene Faenza, William L Blalock

Research output: Contribution to journalReview articlepeer-review


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.

Original languageEnglish
Pages (from-to)1-25
Number of pages25
Issue number11
Publication statusPublished - Nov 21 2021


  • PKR
  • SARS-CoV2
  • TAU
  • beta catenin
  • degenerative disease
  • inflammation
  • interferon
  • small-molecule inhibitors


Dive into the research topics of 'Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis'. Together they form a unique fingerprint.

Cite this