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Rev-erb-? regulates atrophy-related genes to control skeletal muscle mass.

ABSTRACT: The nuclear receptor Rev-erb-? modulates hepatic lipid and glucose metabolism, adipogenesis and thermogenesis. We have previously demonstrated that Rev-erb-? is also an important regulator of skeletal muscle mitochondrial biogenesis and function, and autophagy. As such, Rev-erb-? over-expression 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-? also controls muscle mass. Rev-erb-?-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-? over-expression results in reduced atrogenes expression and increased fiber size. Finally, Rev-erb-? pharmacological activation blocks dexamethasone-induced upregulation of atrogenes and muscle atrophy. This study identifies Rev-erb-? as a promising pharmacological target to preserve muscle mass.

SUBMITTER: Mayeuf-Louchart A 

PROVIDER: S-EPMC5662766 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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The nuclear receptor Rev-erb-α modulates hepatic lipid and glucose metabolism, adipogenesis and thermogenesis. We have previously demonstrated that Rev-erb-α is also an important regulator of skeletal muscle mitochondrial biogenesis and function, and autophagy. As such, Rev-erb-α over-expression 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-α also controls m  ...[more]

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