Glycogen synthase kinase-3 (GSK3): Inflammation, diseases, and therapeutics

Richard S Jope, Christopher J. Yuskaitis, Eleonore Beurel

Research output: Contribution to journalArticle

510 Citations (Scopus)

Abstract

Deciphering what governs inflammation and its effects on tissues is vital for understanding many pathologies. The recent discovery that glycogen synthase kinase-3 (GSK3) promotes inflammation reveals a new component of its well-documented actions in several prevalent diseases which involve inflammation, including mood disorders, Alzheimer's disease, diabetes, and cancer. Involvement in such disparate conditions stems from the widespread influences of GSK3 on many cellular functions, with this review focusing on its regulation of inflammatory processes. GSK3 promotes the production of inflammatory molecules and cell migration, which together make GSK3 a powerful regulator of inflammation, while GSK3 inhibition provides protection from inflammatory conditions in animal models. The involvement of GSK3 and inflammation in these diseases are highlighted. Thus, GSK3 may contribute not only to primary pathologies in these diseases, but also to the associated inflammation, suggesting that GSK3 inhibitors may have multiple effects influencing these conditions.

Original languageEnglish
Pages (from-to)577-595
Number of pages19
JournalNeurochemical Research
Volume32
Issue number4-5
DOIs
StatePublished - Apr 1 2007
Externally publishedYes

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Glycogen Synthase Kinase 3
Inflammation
Pathology
Therapeutics
Medical problems
Mood Disorders
Cell Movement
Alzheimer Disease
Animals
Animal Models
Tissue
Molecules

Keywords

  • Alzheimer's disease
  • Bipolar disorder
  • Cancer
  • Cell migration
  • Diabetes
  • Glycogen synthase kinase-3
  • Inflammation
  • Lithium

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry

Cite this

Glycogen synthase kinase-3 (GSK3) : Inflammation, diseases, and therapeutics. / Jope, Richard S; Yuskaitis, Christopher J.; Beurel, Eleonore.

In: Neurochemical Research, Vol. 32, No. 4-5, 01.04.2007, p. 577-595.

Research output: Contribution to journalArticle

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