MTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation

Jong Seok Moon, Shu Hisata, Mi Ae Park, Gina M. DeNicola, Stefan W. Ryter, Kiichi Nakahira, Augustine M.K. Choi

研究成果: Article査読

222 被引用数 (Scopus)

抄録

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, wedemonstrate thatmTORC1-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 ofRaptor/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.

本文言語English
ページ(範囲)102-115
ページ数14
ジャーナルCell Reports
12
1
DOI
出版ステータスPublished - 2015 7月 7

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学(全般)

フィンガープリント

「MTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル