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J Biol Chem. 2017 Oct 13;292(41):16810-16816. doi: 10.1074/jbc.R117.789628. Epub 2017 Aug 24.

Mitochondrial reactive oxygen species and adipose tissue thermogenesis: Bridging physiology and mechanisms.

Author information

1
From the Dana-Farber Cancer Institute, Harvard Medical School and.
2
Department of Cell Biology, Harvard University Medical School, Boston, Massachusetts 02115.
3
From the Dana-Farber Cancer Institute, Harvard Medical School and bruce_spiegelman@dfci.harvard.edu.

Abstract

Brown and beige adipose tissues can catabolize stored energy to generate heat, relying on the principal effector of thermogenesis: uncoupling protein 1 (UCP1). This unique capability could be leveraged as a therapy for metabolic disease. Numerous animal and cellular models have now demonstrated that mitochondrial reactive oxygen species (ROS) signal to support adipocyte thermogenic identity and function. Herein, we contextualize these findings within the established principles of redox signaling and mechanistic studies of UCP1 function. We provide a framework for understanding the role of mitochondrial ROS signaling in thermogenesis together with testable hypotheses for understanding mechanisms and developing therapies.

KEYWORDS:

adipocyte; adipose tissue; adipose tissue metabolism; mitochondria; reactive oxygen species (ROS); thermogenesis

PMID:
28842500
PMCID:
PMC5641863
DOI:
10.1074/jbc.R117.789628
[Indexed for MEDLINE]
Free PMC Article

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