Class IIa Histone Deacetylases Drive Toll-like Receptor-Inducible Glycolysis and Macrophage Inflammatory Responses via Pyruvate Kinase M2

Kaustav Das Gupta, Melanie R. Shakespear, James E.B. Curson, Ambika M.V. Murthy, Abishek Iyer, Mark P. Hodson, Divya Ramnath, Vikas A. Tillu, Jessica B. von Pein, Robert C. Reid, Kathryn Tunny, Daniel M. Hohenhaus, Shayli Varasteh Moradi, Gregory M. Kelly, Takumi Kobayashi, Jennifer H. Gunter, Alexander J. Stevenson, Weijun Xu, Lin Luo, Alun JonesWayne A. Johnston, Antje Blumenthal, Kirill Alexandrov, Brett M. Collins, Jennifer L. Stow, David P. Fairlie, Matthew J. Sweet*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

34 Citations (Scopus)

Abstract

Das Gupta et al. show that HDAC7 and other class IIa HDAC enzymes control macrophage metabolism. They initiate TLR-inducible glycolysis in these cells and interact with the glycolytic enzyme PKM2 to drive inflammatory responses in vitro and in vivo. Class IIa HDAC inhibitors may have potential for attenuating immunometabolism-linked inflammation.

Original languageEnglish
Pages (from-to)2712-2728.e8
JournalCell Reports
Volume30
Issue number8
DOIs
Publication statusPublished - 25 Feb 2020
Externally publishedYes

Keywords

  • glycolysis
  • histone deacetylases
  • immunometabolism
  • inflammation
  • lysine acetylation
  • macrophage
  • post-translational modification
  • pyruvate kinase
  • toll-like receptor

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