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IL-1 induces mitochondrial translocation of IRAK2 to suppress oxidative metabolism in adipocytes

Authors
  • Zhou, Hao1
  • Wang, Han1, 2
  • Yu, Minjia1, 3
  • Schugar, Rebecca C.1
  • Qian, Wen1
  • Tang, Fangqiang1
  • Liu, Weiwei1
  • Yang, Hui1
  • McDowell, Ruth E.1
  • Zhao, Junjie1
  • Gao, Ji4
  • Dongre, Ashok4
  • Carman, Julie A.4, 5
  • Yin, Mei1
  • Drazba, Judith A.1
  • Dent, Robert6
  • Hine, Christopher1
  • Chen, Yeong-Renn7
  • Smith, Jonathan D.1
  • Fox, Paul L.1
  • And 2 more
  • 1 Cleveland Clinic, Cleveland, OH, USA , Cleveland (United States)
  • 2 Lanzhou University, Lanzhou, China , Lanzhou (China)
  • 3 Harvard Medical School, Cambridge, MA, USA , Cambridge (United States)
  • 4 Bristol Myers Squibb, Princeton, NJ, USA , Princeton (United States)
  • 5 Janssen Research and Development, Spring House, PA, USA , Spring House (United States)
  • 6 University of Ottawa and Ottawa Hospital, Ottawa, Ontario, Canada , Ottawa (Canada)
  • 7 Northeast Ohio Medical University, Rootstown, OH, USA , Rootstown (United States)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Aug 10, 2020
Volume
21
Issue
10
Pages
1219–1231
Identifiers
DOI: 10.1038/s41590-020-0750-1
Source
Springer Nature
License
Yellow

Abstract

Obesity is often accompanied by chronic inflammation. Li and colleagues show that, in mice fed high-fat diets, IL-1 signaling in adipocytes induces an unconventional IRAK2 translocation to mitochondria and suppresses respiratory super-complex formation to alter mitochondrial function, and exacerbates obesity.

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