Nobiletin fortifies mitochondrial respiration in skeletal muscle to promote healthy aging against metabolic challenge.

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ID: 31173
2019
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Abstract
Circadian disruption aggravates age-related decline and mortality. However, it remains unclear whether circadian enhancement can retard aging in mammals. We previously reported that the small molecule Nobiletin (NOB) activates ROR (retinoid acid receptor-related orphan receptor) nuclear receptors to potentiate circadian oscillation and protect against metabolic dysfunctions. Here we show that NOB significantly improves metabolic fitness in naturally aged mice fed with a regular diet (RD). Furthermore, NOB enhances healthy aging in mice fed with a high-fat diet (HF). In HF skeletal muscle, the NOB-ROR axis broadly activates genes for mitochondrial respiratory chain complexes (MRCs) and fortifies MRC activity and architecture, including Complex II activation and supercomplex formation. These mechanisms coordinately lead to a dichotomous mitochondrial optimization, namely increased ATP production and reduced ROS levels. Together, our study illustrates a focal mechanism by a clock-targeting pharmacological agent to optimize skeletal muscle mitochondrial respiration and promote healthy aging in metabolically stressed mammals.
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nohara2019nobiletinnature Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Nohara, Kazunari;Mallampalli, Venkata;Nemkov, Travis;Wirianto, Marvin;Yang, Jiah;Ye, Youqiong;Sun, Yuxiang;Han, Leng;Esser, Karyn A;Mileykovskaya, Eugenia;D'Alessandro, Angelo;Green, Carla B;Takahashi, Joseph S;Dowhan, William;Yoo, Seung-Hee;Chen, Zheng;
Journal Nature communications
Year 2019
DOI
10.1038/s41467-019-11926-y
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