MTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation Academic Article uri icon


MeSH Major

  • Carrier Proteins
  • Glycolysis
  • Hexokinase
  • Inflammasomes
  • Multiprotein Complexes
  • TOR Serine-Threonine Kinases


  • The mammalian target of rapamycin complex 1 (mTORC1) regulates activation of immune cells and cellular energy metabolism. Although glycolysis has been linked to immune functions, the mechanisms by which glycolysis regulates NLRP3 inflammasome activation remain unclear. Here, we demonstrate that mTORC1-induced glycolysis provides an essential mechanism for NLRP3 inflammasome activation. Moreover, we demonstrate that hexokinase 1 (HK1)-dependent glycolysis, under the regulation of mTORC1, represents a critical metabolic pathway for NLRP3 inflammasome activation. Downregulation of glycolysis by inhibition of Raptor/mTORC1 or HK1 suppressed both pro-IL-1β maturation and caspase-1 activation in macrophages in response to LPS and ATP. These results suggest that upregulation of HK1-dependent glycolysis by mTORC1 regulates NLRP3 inflammasome activation.

publication date

  • January 2015



  • Academic Article



  • eng

PubMed Central ID

  • PMC4858438

Digital Object Identifier (DOI)

  • 10.1016/j.celrep.2015.05.046

PubMed ID

  • 26119735

Additional Document Info

start page

  • 102

end page

  • 15


  • 12


  • 1