Chouchani Edward T, Kazak Lawrence, Spiegelman Bruce M
From the Dana-Farber Cancer Institute, Harvard Medical School and.
Department of Cell Biology, Harvard University Medical School, Boston, Massachusetts 02115.
J Biol Chem. 2017 Oct 13;292(41):16810-16816. doi: 10.1074/jbc.R117.789628. Epub 2017 Aug 24.
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.
棕色脂肪组织和米色脂肪组织能够分解储存的能量以产生热量，这依赖于产热的主要效应因子：解偶联蛋白1（UCP1）。这种独特的能力可被用作治疗代谢性疾病的方法。现在，众多动物和细胞模型已经证明，线粒体活性氧（ROS）发出信号以支持脂肪细胞的产热特性和功能。在此，我们将这些发现置于氧化还原信号传导的既定原则和UCP1功能的机制研究背景中。我们提供了一个框架，用于理解线粒体ROS信号传导在产热中的作用，以及用于理解机制和开发治疗方法的可测试假设。
