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

被引:77
作者
Chouchani, Edward T. [1 ,2 ]
Kazak, Lawrence [1 ,2 ]
Spiegelman, Bruce M. [1 ,2 ]
机构
[1] Harvard Med Sch, Dana Farber Canc Inst, Boston, MA 02115 USA
[2] Harvard Univ, Dept Cell Biol, Sch Med, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
adipocyte; adipose tissue; adipose tissue metabolism; mitochondria; reactive oxygen species (ROS); thermogenesis; DIET-INDUCED OBESITY; BROWN-FAT MITOCHONDRIA; INSULIN SENSITIVITY; UNCOUPLING PROTEINS; ENERGY-EXPENDITURE; OXIDATIVE-PHOSPHORYLATION; ISOCITRATE DEHYDROGENASE; PROTON CONDUCTANCE; DIVERGENT ROLES; MICE LACKING;
D O I
10.1074/jbc.R117.789628
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:16810 / 16816
页数:7
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