期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-14596-2
关键词
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资金
- INSERM
- Contrat Plan Etat Region (CPER)
- Region Nord Pas-de-Calais/FEDER
- EU consortium Eurhythdia (FP7)
- ANR-Labex-EGID (EGID) [ANR-10-LABX-46]
- EFSD (European Foundation for the Study of Diabetes)-Eli Lilly
- Fondation Francophone pour la recherche sur le diabete (FFRD)
- Federation Francaise des Diabetiques (AFD)
- AstraZeneca
- Eli Lilly
- Merck Sharp Dohme (MSD)
- Novo Nordisk
- Sanofi
- 'ERC-Region Hauts de France' grant
- Fondation de France
- Association Francaise contre les Myopathies (AFM)
The nuclear receptor Rev-erb-alpha modulates hepatic lipid and glucose metabolism, adipogenesis and thermogenesis. We have previously demonstrated that Rev-erb-alpha is also an important regulator of skeletal muscle mitochondrial biogenesis and function, and autophagy. As such, Rev-erb-alpha overexpression in skeletal muscle or its pharmacological activation improved mitochondrial respiration and enhanced exercise capacity. Here, in gain-and loss-of function studies, we show that Rev-erb-alpha also controls muscle mass. Rev-erb-alpha-deficiency in skeletal muscle leads to increased expression of the atrophy-related genes (atrogenes), associated with reduced muscle mass and decreased fiber size. By contrast, in vivo and in vitro Rev-erb-alpha over-expression results in reduced atrogenes expression and increased fiber size. Finally, Rev-erb-alpha pharmacological activation blocks dexamethasone-induced upregulation of atrogenes and muscle atrophy. This study identifies Rev-erb-alpha as a promising pharmacological target to preserve muscle mass.
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